This was written by one of our fine residents, who will soon be an EMS fellow: Michael Perlmutter
Case
A mid-50s male came to the ED with a burning sensation that was acutely worse while at home. He had recently returned from overseas travel where these symptoms had been intermittently bothersome over the preceding weeks and had been attributed to heartburn.
The previous evening, he was at rest and developed severe pain with associated shortness of breath, diaphoresis and a brief syncopal episode. He had ongoing pain following the syncopal event but went to bed and awoke in the morning with ongoing pain.
He came to the ED at the urging of his wife. At ED presentation, he was asymptomatic but developed extremely brief periods of recurrent burning discomfort that were centered about the sternal notch.
Given his history, an EKG, labs including high sensitivity troponin, and chest radiograph were ordered.
Smith: this was shown to me without any other information, and I said that it is strongly suggestive of inferior OMI, probably reperfused. There is minimal STE in lead III with reciprocal STD in aVL. The terminal part of the T-wave is inverted in lead III, and reciprocally terminally upright in lead aVL.
I put this through the Queen of Hearts and was shocked that she did not see it.
Case continued
A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. His initial high sensitivity troponin I returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonary embolism and aortic aneurysm or dissection but this too was unrevealing. Another EKG was also obtained.
ECG at time 82 minutes:
What do you think?
Smith: all STE in lead III is gone, as is the STD in aVL. This dynamic change is diagnostic of ACS. And so, of course, is the elevated troponin.
Cardiology was consulted and agreed that his history was high risk for ACS and a next-day angiogram was merited. He was started on intravenous heparin and given aspirin. His care was signed out to the overnight team with a plan to continue to obtain serial troponin measurements and admit the patient to the hospital for an angiogram.
Overnight, his troponin continued to rise, but he remained asymptomatic and was resting between cares. When pressed, he endorsed mild, very brief periods of a retrosternal burning sensation and serial ECGs were obtained.
time zero: 1378
1 hours: 1436
4 hours: 1651
6 hours: 1750
8 hours: 1850
Smith: But rising troponins only tell you about the past, not about the present moment!!
ECG at 8.3 hours
What is noticeable now?
The first EKG was concerning for a Wellen’s-like pattern of subtle reperfusion changes in the setting of stuttering anginal-equivalent symptoms, but none were diagnostic of STEMI or OMI.
Later in the night, the patient became bradycardic and developed a Mobitz II pattern, but he remained asymptomatic and hemodynamically stable. Very early in the morning, he reported recurrence of a heartburn sensation, so another EKG was obtained.
ECG at 9 hours:
Smith: the STE with reciprocal STD in aVL is back. In addition, there are now hyperacute T-waves in the inferior leads. There is also a bit of new ST Elevation in right precordial leads: is there also some Right ventricular involvement?
This was also non-diagnostic for OMI, although the dynamic changes are diagnostic of ACS. However, with the development of Mobitz II and ongoing stuttering symptoms, the 12-lead EKG was left attached to the patient and was observed.
After about 10-15 minutes, there was a significant change and very large inferior ST elevation with reciprocal ST depression in the lateral leads was observed and the patient was moved to the stabilization room.
ECG at 11 hours:
Given this EKG with diagnostic findings, his heparin infusion was stopped, and he was given a 5000 unit heparin bolus and 180 mg of ticagrelor while the cardiac catheterization laboratory was activated and interventional cardiology was emergently consulted.
Angiography was performed and found a normal LAD, a large co-dominant LCX, and 95% disease at the mid-RCA. A large RPDA and a small RPAV giving rise to RPL1 was seen. The RCA was stented successfully with TIMI III flow noted post-procedure and the patient has done well with a post-PCI TTE demonstrating good LVEF and no wall motion abnormality. Given the right coronary anatomy seen during angiography, it is particularly interesting that subtle T wave changes were seen on the previous EKGs in the high lateral leads that would otherwise only be expected with a more proximal RCA lesion.
This case highlights the importance of maintaining a high degree of suspicion for clinically important disease even in the absence of classic symptoms or an EKG without STEMI despite an initially high troponin.
This case highlights the value of continuous 12-lead EKG monitoring, which is not routinely available in many institutions but proved invaluable in making a timely diagnosis at the time that the EKG became diagnostic.
Smith: There is a misconception that uptrending troponin had an effect on the decision to go to the cath lab. It really should have little influence on us. A rising troponin just tells us what was happening hours ago. A good size infarct that no longer has active ischemia will have continually rising troponins due to the damage that was done hours ago. The only way to know if this patient whom you know has Acute MI needs the cath lab is if 1) symptoms are present and can't be controlled or 2) the ECG shows active ischemia. Also: electrical instability, pulmonary edema, or hypotension.
In this case, there was electrical instability (Mobitz II block). That alone is enough to activate the cath lab.
This apparently did not prompt cath lab activation, but it did lead to continuous ECG monitoring which led to the ECG which mandated cath lab activation.
MY Comment, by KEN GRAUER, MD (12/3/2024):
- The 1st question that arises — Is whether or not either of the first 2 ECGs might be diagnostic of an acute inferior OMI?
- Perhaps the more clinically important question is — How can we learn retrospectively what might have been done better. While fully acknowledging that, "Hindsight is 100% in the retrospectoscope" (ie, from the comfort of my computer desk chair) — I think it insightful to relook at the 4 serial tracings shown in this case.
- NOTE: Mention is made that a total of 10 serial ECGs were recorded in today's case over an 11-hour span. I only have access to the 4 ECGs that I show in Figure-1 — plus the final ECG done at T = 11 hours, at which time dramatic and diffuse hyperacute ST elevation is seen. I limit my comments to the history provided and the 4 ECGs shown in Figure-1.
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| Figure-1: I've labeled the first 4 ECGs shown in today’s case. |
- Given this history (with the intermittent nature of this patient's symptoms) — anything might be seen on the initial ECG. It is therefore important to realize that even IF this patient was having an ongoing cardiac event — We might not necessarily see obviously acute changes.
- Instead, what might be seen — is a certain amount of "pseudo-normalization" (ie, if some degree of spontaneous reperfusion had at some point occurred). We should therefore be prepared to look for subtle ECG findings that may be important — with need to correlate the presence and severity of symptoms with each of these serial ECGs in order to optimally understand what happened.
The rhythm in ECG #1 is sinus at ~65/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.
- As will become important momentarily — the PR interval = 0.20 second in ECG #1 — the frontal plane axis = +50 degrees — and the patient had no CP at the time this tracing was recorded.
- In ECG #1 — 3 leads show findings of potential concern: i) The most concerning finding is seen in lead III (within the RED rectangle) — in which there is slight-but-real ST elevation (RED arrow), with a biphasic T wave ending in terminal negativity.
- ii) That this ST-T wave abnormality is "real" — is supported by reciprocal changes in high-lateral leads aVL and I (BLUE arrows highlighting ST segment straightening, with a hint of ST depression in these leads).
- In the chest leads — there is T wave "imbalance", in that the upright T wave in lead V1 is taller than the upright T wave in lead V6. As I emphasize in My Comment in the June 1, 2022 post in Dr. Smith's ECG Blog — such "T wave imbalance" is a nonspecific finding that I have on occasion found useful as a "tip-off" to an acute coronary syndrome that I might not otherwise have recognized.
- BOTTOM Line: While I found interpretation of ECG #1 to be non-diagnostic for OMI as a single tracing — given the history, I thought the subtle abnormal findings in leads I,III,aVL and the precordial T wave "imbalance" — could reflect a certain amount of "pseudo-normalization" (from spontaneous reperfusion) in a patient with a recent event, especially since the patient had no CP at the time ECG #1 was recorded!
- Suggestion: Given how quickly ECG findings may change in an acute coronary syndrome of uncertain duration — I favor not waiting more than ~20 minutes for the initial repeat ECG (with additional repeat tracings in short succession until there is clear indication of no progression).
- My reason for noting the slight shift in frontal plane axis in ECG #2 (ie, from +50 to +70 degrees) — is because there is subtle-but-real change in ECG appearance for the leads mentioned above in ECG #1 — and we want to ensure that a change in frontal plane axis is not responsible for this (I did not think this slight change in axis was the cause for the change in limb lead ST-T wave appearance).
- Specifically: i) Despite no significant difference in QRS morphology — there is no longer any ST elevation in lead III; — and, ii) There is no longer any hint of ST depression in leads I and aVL — and T wave amplitude has increased slightly in both of these leads.
- While fully acknowledging the subtlety in these limb lead ST-T wave changes — the fact that 3 leads show similar evolution to me suggests that these changes are "real" — and may reflect "dynamic" ST-T wave change. Given the elevated Troponin (= 1300 ng/L) — Hasn't the diagnosis of acute OMI (and the need for prompt cath) been made?
- Despite no more than slight axis adjustments — the limb leads in ECG #3 and ECG #4 continue to show ongoing changes of coronary reperfusion. These include: i) Progressive increase in T wave amplitude in leads III and aVF (compared to ECG #2); — and, ii) Progressive decrease in T wave amplitude in lead aVL (compared to ECG #2).
- Note the serial change in the ST-T wave appearance in lead V1 over the course of the 4 ECGs in Figure-1. Although we usually associate development of a Wellens'-like sharp T wave descent into terminal T wave negativity in leads V2,V3,V4 with Wellens' Syndrome — here we see this evolution only in lead V1. In retrospect — I interpreted these serial lead V1 ST-T wave changes as support of the early precordial T wave "imbalance" as a "tip-off" finding that I noted when interpreting ECG #1.
- Note also development of distinct J-point notching in leads V3,V4 that was not seen earlier. As per My Comment in the February 2, 2024 post — knowing the results of today's cardiac catheterization, I retrospectively interpreted this finding as representing ischemic Osborn waves.
- Today's patient was found on cath to have RCA OMI. Mobitz I is common in this clinical setting. Mobitz II is not. This is especially true because: i) The QRS complex is narrow in all 4 ECGs seen in Figure-1 (whereas the QRS is usually wide with Mobitz II); — and, ii) The first 2 ECGs in today's case show a normal PR interval ( = 0.20 second) — whereas ECG #3 and ECG #4 now show 1st-degree AV block (PR interval = 0.24 second). It is common for Mobitz I in the setting of inferior OMI to evolve from a normal PR interval — to 1st-degree AV block — to 2nd-degree, Mobitz I. This sequence of evolution is not seen with Mobitz II — that typically presents with abrupt failed conduction despite a constant (and usually normal) PR interval.
- What most likely was seen during the night — was 2nd-degree AV block with 2:1 AV conduction, which is often mistakenly interpreted as Mobitz II (because the PR interval remains constant as every-other-beat is non-conducted). Technically — one can not distinguish between Mobitz I vs Mobitz II when there is 2:1 AV conduction — because you never see 2 consecutively conducted beats (so you never know whether the PR interval would progressively increase before dropping a beat IF given a chance to do so). That said — in the setting of acute inferior OMI with a narrow QRS and evolution from a normal to a prolonged PR interval — the odds that 2:1 AV block represent Mobitz I are overwhelming. (For more on ECG recognition and clinical significance of 2nd-degree AV blocks — Please check out My Comment at the bottom of the page in the November 12, 2024 post in Dr. Smith's ECG Blog).
- Clinical Relevance: On seeing PR interval lengthening during the night — that evolved into 2:1 AV block — We had at that time, yet one more piece of evidence diagnostic of acute inferior OMI in progress.
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