Palpitations and Chest Tightness: Should You Activate the Cath Lab (or Give Thrombolytics)?

This case was sent by Jessica Carmichael, and Emergency Physician  on active duty at Irwin Army Community Hospital in Fort Riley, Kansas.  She trained at Brooke Army Medical Center.

ECG and Case

I was sent this ECG with some information, but I looked only at the ECG before reading the text:

What do you think?

My response was this:

"I have not read the text of your email yet, but I would say that this is benign normal variant STE."

(There is also atrial fibrillation without a rapid ventricular response.)

"Now I will read your text:"

Here is the text:

"The following ECG was sent to me by a former resident yesterday and seems timely given your recent post [You Diagnose Pericarditis at your Peril (at the Patient's Peril!)]. The resident was berated by cardiology for activating the cath lab as he felt it was obviously pericarditis. I was concerned that there wasn't a truly discernible J or S wave in V3 [note: there is both a J-wave and an S-wave in V3, so there is NOT terminal QRS distortion]. Given that there is no acceptable miss rate for MI, I felt activating the cath lab was absolutely appropriate."

This was my response:

It is NOT pericarditis.  It is normal variant.

It is reasonable to activate. I would have instead done a contrast echo to prove no wall motion abnormality.

Comment: The very high QRS voltage, the very marked J-waves in many leads, and the short QT interval make this very unlikely to be LAD occlusion.  But it does meet STEMI "criteria" in multiple leads.

Here is the full history:

"Basics: 28 yo AA male who had a history of WPW who had sudden onset of heart palpitations and chest tightness 5/10 at rest. Had had ablation in 2016. No issues since. Presented with no other associated ROS, save for lightheadedness. Denies drug use, UDS neg. No family history.  Physically fit. Systolic BP 112. Sats normal.  Takes daily beta blocker. Denied recent illness, exertional chest pain or fever. No PE risk factors." 

"Found to be in new afib with multiple concerning EKGs.  Rate from 50s to 80s, irregular."

"Old EKG with early repol, but in my opinion new EKG much more drastic/changed." 

"Called a STEMI and discussed with cards who initally advised me of early repol findings. Requested they evaluate EKG. After, they remarked it looked like pericarditis, which I argued didn’t fit the clinical picture. He admitted the EKG was abnormal but was skeptical. Went ahead with our protocol for him to get heparin, TNKase, plavix, ASA and flew to outlying hospital." 

"Initial troponin about 1 hour after symptom onset was neg. CKMB was mildly elevated at 2.5 ish. CK 1300. After the pericarditis statement by cards, I added CRP and ESR after patient left, which came back negative.  Unfortunately, didn’t think to do a bedside echo before he left. "

"Cards texted me later and said he was fine, still in afib and that they felt his EKG was unchanged from old and consistent with early repol.  Cath lab deferred. Didn’t get report on if second troponin was done. "

Happy to get further follow up? I have about 4 EKGs from his brief stay in my ER as well as a one previous from his records. 

Found the recent blog post interesting in light of this case!
[You Diagnose Pericarditis at your Peril (at the Patient's Peril!)]

Jessica Carmichael, MD

Further analysis:

Dr. Carmichael performed 4 serial ECGs and they were all unchanged.   The QTc was between 385 ms and 402 ms.

Here is one of them:

No significant change
Notice the computer calls it pericarditis.
On other identical ECGs in the same series, the computer calls it ***STEMI***

What if we had used the 3- or 4-variable formulas?

STE60V3 = 4 mm

RAV4 = 33 mm

QTc = 400 ms

QRSV2 = 15 mm

3-Variable: = 17.62, which is far below the cutoff of 23.4

4-Variable: = 13.93, which is far below the cutoff of 18.2

The formulas would have predicted benign normal variant STE (early repol).

Outcome

Angiogram was normal.

All trops negative.

By the way this is NOT pericarditis.

Learning Points:

1. It is never acceptable to berate another physician who is doing their best for the patient.  Obviously Dr. Carmichael was providing excellent care.

2. This ECG clearly meets STEMI "criteria" of 2.5 mm of STE in 2 consecutive right precordial leads, in addition to meeting STEMI criteria of 1 mm in lateral leads.

3.  There are features that can clue you in to benign ST Elevation: High voltage, profound J-waves, and short QT

4. Use the formulas.  They are very helpful.  (by the way, the formulas have now been externally validated in a large cohort; publication pending.  The 4-variable formula is now proven as the best!!)

5. One can avoid angiogram by performing a formal contrast echo.  Had Dr. Carmichael had access to one and been able to perform it, it would have shown no wall motion abnormality.  This would have ruled out LAD occlusion as the etiology of the STE, and she would have been able to avoid giving potentially harmful TNK-tPA.

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Comment by KEN GRAUER, MD (6/26/2018):

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Interesting case and write-up submitted by Dr. Jessica Carmichael — with excellent Comments by Dr. Smith. The concern was ST elevation felt to be significantly more than on a previous tracing. As a result, a STEMI was called. Cardiology initially favored acute pericarditis.

• As per Dr. Smith — features suggesting this was not an acute OMI ( = Occlusion-related Myocardial Infarction) include the very high QRS voltage; the very marked J-waves in multiple leads; the short QTc — and extremely low values in Dr. Smith’s 3- and 4-variable formulas. That said, given ST elevation with new symptoms — diagnostic cath was reasonable. That said, given the above ECG features — obtaining an Echo during symptoms that failed to show wall motion abnormality could have avoided a cath ...

For the purpose of academic discussion — I’ll add the following thoughts:

• The principal factor that prompted cath lab activation was concern that the ST elevation in Figure-1 was significantly increased from a prior ECG that showed early repolarization. Cardiology later thought there was no significant change between the 2 tracings. While impossible to comment on this comparison (since we are not given the prior ECG) — caveats to be aware of that may affect lead-to-lead comparison of serial tracings, are the need to make note of any change in: i) frontal plane axis; ii) in R wave progression; and, iii) in QRS amplitude in the various leads. Change in any of these features complicates judgment about serial differences. Clearly, the amount of ST elevation seen in Figure-1 is marked (at least 4mm in lead V3). But QRS amplitude in leads V3-through-V6 is also dramatically increased (off the page in lead V4, and overlapping neighboring leads in V3, V4, V5). As a result, the amount of ST elevation relative to QRS amplitude in a given lead is proportionately not so excessive. Was QRS amplitude equally large as it is here on the prior tracing?
• The History is KEY in this case. As per Dr. Carmichael — “sudden onset of heart palpitations and chest tightness at rest” is not a typical history for acute pericarditis. Often overlooked is awareness that new-onset arrhythmias (including faster SVT rhythms, as well as slow AFib) may present to the ED as chest discomfort. It would be interesting to know more about the nature of this patient’s chest pressure and palpitations — including whether both started at the same time, whether both were ongoing in the ED, and whether the patient was aware of when he had a regular vs irregular heart rate. Such historical information can sometimes prove invaluable in suggesting when chest discomfort might be the result an arrhythmia.
• An additional ECG feature against the diagnosis of acute pericarditis is the finding in lead V2 of beginning T wave inversion at the same time that there is still significant ST elevation in this lead (BLUE arrows within the blue rectangle in Figure-1). With the typical evolution of acute pericarditis — ST segments first return to the baseline before T wave inversion occurs. In contrast — T wave inversion at the same time as there is ST elevation is common with acute infarction, and may be seen in some types of repolarization variants.
• Additional ECG features against acute OMI — are how generalized the ST elevation is, and the lack of reciprocal ST-T wave depression. Granted, reciprocal ST depression is not always present with OMI — and it is possible to have OMI superimposed on a baseline tracing of early repolarization … This is the reason access to Echo in the ED at the time of symptoms is so valuable. In view of a predominance of ECG features in this case against OMI — the absence of a wall motion abnormality on Echo obtained during symptoms would essentially rule out OMI.

Figure-1: Initial ECG obtained in the ED on a 28-year old man with new symptoms (See text for details).

Final Thought: Is there group beating in Figure-1? This 28yo man has a history of WPW with prior ablation — but presumably was in sinus rhythm prior to the day of admission. He is now in AFib at a surprisingly low heart rate for new-onset of this arrhythmia. Is the dose of ß-blocker that he is on high enough to produce this much heart rate slowing with new AFib? Or could there be Wenckebach block out of the AV node, resulting in the similar short-long cycling for the first 5 beats in Figure-1 — with Wenckebach periodicity also seen toward the end of the rhythm strip (ie, progressively decreasing R-R intervals from beats #7-thru-10; and similar duration pauses between beats #2-3; 4-5; 6-7; 10-11 that are all less than twice the shortest R-R interval). 

• Clearly, a longer period of monitoring is needed to know for sure — and the suggestion of group beating that we see could all be coincidence. But it IS worthwhile pointing out that recognition of group beating with atrial fibrillation or atrial flutter should suggest the possibility of Wenckebach conduction out of one or more levels within the AV node.