MY Comment, by KEN GRAUER, MD (12/13/2022):
===================================
- XXXXXX
-USE.png) |
| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
XXXXX
A 60-something male complained of episodes of chest pain.
The troponins were "negative." High sensitivity Abbott Artchitect at time zero was 4 ng/L and at 2 hours was 5 ng/L. URL for this assay is 34 ng/L in men. Thus, Acute MI was ruled out, and it was ruled out with VERY low troponins.
We can discharge the patient, right?
I had not seen the ECG at this point, but the residents had not seen any ischemia. I said, "Well, how long are the episodes of chest pain?"
They did not know the answer, so I went with the med student to ask. The patient stated that no episode, including today's, had lasted longer than 15 minutes.
He also confirmed that he had had chest pain at the time of the ECG recording.
He mentioned that his chest pain was worse when he rolled to the side, and when taking a breath. But it was not at all tender to my exam.
I said to the residents that you have not ruled out unstable angina if troponins are negative but the chest pain was only brief. Brief ischemia with pain might not lead to troponin elevation.
For such patients, it can be useful to use "Risk Scores" such as HEART or EDACS. I prefer EDACS for many reasons:
1. Age is in 5 year increments. With HEART score, age of 46 = 64, and that is absurd.
2. The "E" and "T" in HEART score: if the ECG is ischemic, or the Troponin is elevated, then the patient needs admission regardless of the remainder of the score.
3. That leaves "H" and "R". We know from many studies that risk factors are only important in young people. And the EDACS derivation confirmed this. Which is why EDACS does not take risk factors into account for patients over age 50.
4. That leaves "H". "H" is very subjective, and this is great for someone who knows the chest pain literature and has a lot of experience. But what about for those with less knowledge? EDACS has such factors as "Reproducible" "Radiation" "Worse with inspiration" and "diaphoresis".
5. Finally, EDACS is completely independent of the ECG and Troponin. If either are "positive," the patient needs further evaluation.
So when I teach use of the risk scores, I prefer EDACS.
This patient EDACS score was 19. A score of 16 or above SHOULD BE "OR BELOW" RIGHT? in the presence of a non-ischemic ECG and 2 (4th or 5th generation) troponins below the 99th percentile confers a ＜1% risk of 30-day adverse events. High sensitivity troponins that are very low result in a 99.7% NPV!
But this patient's score is 19. With very low troponins, his risk is probably less than 1%.
But that is ONLY if the ECG is non-ischemic.
So I went to look for the ECG:
There is ST depression in V3-V5.
============================
- The truism, "What goes up must come down" — applies not only to life phenomena — but also to the course of ST segment deviations during the evolution of an acute OMI (as per the above Figure in which Dr. Meyers reviews the ECG findings of OMI progression).
- As experienced ECG interpreters charged with overseeing the interpretation of others — overreading tracings without the benefit of clinical information is the unenviable task we face all the time. This can be challenging — and today's case emphasizes how difficult this can be when the tracing placed before us was obtained during the period of "pseudo-normalization".
- What is the History?
- What is "Normal"?
- KEY: If the ECG in question was obtained from an acute care center or from an EMS directory — then the chances increase greatly that the history may entail, "new-onset chest pain" — in which case awareness of the "pseudo-normalization" stage of acute OMI progression should prompt us to lower our threshold for pulling the patient chart and/or immediately contacting the interpreting clinician. Failure to do so may result in overlooking subtle ST-T wave changes in a patient "in passage" from a frank STEMI toward reperfusion changes.
- There is significant baseline artifact in ECG #2, especially in the limb leads. While this does not prevent interpretation of this tracing — it does make assessment of limb lead ST-T wave findings more difficult. Hopefully, effort will be made in follow-up tracings to minimize (as much as possible) this artifact.
- There appears to be subtle-but-real ST elevation in leads III and aVF (ie, with respect to the dotted RED baseline I drew in these leads). While this is clearly not diagnostic (especially given the absence of reciprocal ST depression in lead aVL) — it could be important.
- Despite the artifact in leads I and aVL — the ST segments in these leads appear to be flat (as suggested by the parallel BLUE lines). Again — while nondiagnostic and clearly nonspecific — this is not a "normal" finding.
- Similar nonspecific (and nondiagnostic) ST segment straightening is present in leads V3-thru-V6. This subtle-but-real finding could be relevant, depending on the history. For example — the ST segment in leads V2,V3 should normally manifest a gentle upsloping until it joins the upright T wave in these leads. Instead — the parallel BLUE line in lead V3 of ECG #2 shows abnormal (albeit subtle) ST straightening.
POINT #3: When T waves in each of the chest leads are upright (as they are in ECG #2) — the T wave in lead V1 is usually not taller than the T wave in lead V6. This "imbalance of precordial T waves" is not seen very often — and in the “right” clinical setting, has been associated with recent OMI from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM).
- NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized (For 3 more examples of this finding — See My Comments at the bottom of the page in the October 23, 2020 post — the March 26, 2022 post — and in the June 1, 2022 post of Dr. Smith's Blog).
- To Emphasize: As an isolated finding — I might not think much of the surprisingly tall T wave in lead V1 of ECG #2 (which by itself in an asymptomatic patient, could be a normal variant). But given that this T wave in lead V1 is so much taller than the T wave in lead V6 (as per the BLUE arrows in Figure-1) — and given the subtle ST-T wave findings I described above in no less than 8/12 leads — I would want to know the History (and see additional tracings done on this patient) before I would render my interpretation.
-USE.png) |
| Figure-1: I've reproduced and labeled the initial ECG that was shown in today's post (See text). |
=============================
===================================
- The reason it's important to go through this soul-searching process — is so that we can learn from mistakes made, in order to optimize care in the future.
- Great point by Drs. Smith and McLaren to emphasize that “Wellens’ Syndrome” does not only occur in the anterior leads. Although the distribution of the LAD is the most common place to see the reperfusion ST-T wave changes of Wellens’ Syndrome — this 1st Case illustrates what an Infero-Postero Lead Wellens’ Syndrome looks like.
- KEY Point: The history we were told in Case #1 was “3 weeks of intermittent non-exertional chest pain without associated symptoms”. But not only was the initial ECG misinterpreted — the fact that the history was summarized as “3 weeks of intermittent chest pain” indicates that the treating clinicians failed to understand both the expected ECG findings, as well as the required time course for symptoms when there is a process such as occurs with true "Wellens' Syndrome".
- This is relevant — because it invalidates the “History” component of the HEART and EDACS scores that were said to be "low risk". As per Drs. McLaren and Smith — the initial ECG in Case #1 shows that an event did occur. The question is WHEN? Although diagnostic — ECG changes in the initial tracing in Case #1 (as well as the History) suggest days, or even up to 2-3 weeks earlier might be the timing of the event — in which case Troponin should not necessarily be expected to be elevated.
- WHAT brought this 1st patient to the ED on the day he presented — which was no less than 3 weeks after the onset of his symptoms? While fully realizing that we can't write a "book-long history" on all patients — striking for its absence is any mention in the History regarding symptoms on the day he presented (and at the time the initial ECG was obtained). Optimal clinical ECG interpretation depends on correlation with the timing, duration and severity of symptoms.
- I always believed not to do a low-level ETT after a completed (stable) MI under observation (ie, in the hospital) before the patient goes home — is to allow the patient to do their own "unmonitored Stress Test” once they get home.
- That said — my experience having taught ambulatory Stress Testing for 3 decades, has always been that the most difficult part of correctly performing an ETT — is knowing the extent to “push” (encourage) the patient — and — learning WHEN to stop the test. I’ve always been impressed at how quickly a patient can go from easily tolerating activity on the treadmill — to virtual collapse no more than moments later.
- So — performing an ETT on this patient in Case #1 would not necessarily be contraindicated IF the test was performed with the proper caution (which in Case #1 means fully appreciating that this patient has had a recent event!).
- Concerning for its absence in the History we were given is any mention about WHEN during the Stress Echo (ie, at what time and at what activity level during the test) was “inducible ischemia” seen? Was this objective evidence of inducible ischemia accompanied by chest pain?
- If objective ECG and Echo evidence of induced ischemia occurred within the first few minutes of low-level exercise — then even IF the clinicians failed to appreciate that this patient’s initial ECG was diagnostic for a recent event — there is NO WAY this patient should have had to wait 2 weeks for an “elective angiogram”. The cardiologists I used to work with would have admitted that patient for cath the next day.
- And IF it turned out that despite inducible ischemia (on Echo and ECG) at low-level exercise, that this patient did not have any chest pain — then this is the definition of “Silent" Ischemia. It might explain why this patient took 3 weeks to show up in the ED in the first place (because at least some — or perhaps most of the time, the patient may have been unaware of symptoms during activities of daily living). In that case — what might happen with all of the inducible “silent” ischemia episodes (ie, without symptoms) that would be bound to occur over the 2 weeks until the “elective” cath was finally done?
To Be CLEAR: I am not saying that a Stress Test should have been done on this patient in Case #1. There should have been better appreciation of the History to be looked for — and ECG reperfusion changes from recent infarction should have been recognized — such that optimal care would have entailed prompt cath with a preventive intervention. I am simply saying that when done properly — Stress Testing can be safe done 10 days after a stable MI.
=====================
- Details of the History are again lacking — because an ECG had been obtained 2 months prior, yet we do not know the reason WHY this prior ECG was done.
- KEY Point: Without knowing anything about this 60-year old patient's prior medical history — the story we are given (ie, 3 weeks of exertional chest pain — but painfree on presenting to the ED) — provides the definition of angina pectoris. And IF this is the 1st time that this 60-year old is having exertional chest pain — then this fits the definition of "unstable" angina.
- But I wanted to comment on this 2nd patient's initial ECG — which apparently was read as "normal" (Figure-1).
-USE%20copy.png) |
| Figure-1: I have reproduced and labeled the 4th ECG shown in Today's Blog Post. This ECG is from Case #2. It was obtained ~2 months prior to this patient's presentation in the ED. |
- The rhythm is sinus at ~65/minute. Intervals (PR, QRS, QTc) and the axis is normal. There is no chamber enlargement.
- Regarding Q-R-S-T Changes — There is a tiny q wave in lead aVL. R wave progression is normal. It is the ST-T wave changes that are of concern.
- The normal ST segment manifests a gentle upsloping until it blends almost imperceptibly into the T wave. Instead — there is subtle-but-real ST segment straightening in multiple leads in Figure-1 (schematically shown by the parallel RED lines).
- If anything — there is usually slight (normal) ST elevation in leads V2 and V3. Not only is this normal slight amount of ST elevation missing in these 2 leads — but J-point ST depression is present beginning in lead V3 — and persisting to lead V6 (BLUE arrows).
- We were not told whether this patient was having symptoms at the time the ECG in Figure-1 was obtained. But we know that he had typical angina 5 weeks later, which then persisted for 3 more weeks until he finally presented to the ED.
- There is an "art" to eliciting the History. There are many ways to ask the questions. IF this patient in Case #2 was in fact having typical anginal symptoms at the time the ECG in Figure-1 was obtained — this should have prompted at the very least some Stress Test (if not cardiac cath) — which if done, could possibly have prevented the large infarction he subsequently had.
No comments:
Post a Comment