This ECG was texted to me on my phone, with the words "Asymptomatic with hyperthyroidism:"
I replied that precordial leads are misplaced and to record it again.
How did I know this? There are well formed R-waves in V1, but none in V2 and V3, then they return in V4. It is possible that there is focal infarction over V3 and V4, but very unlikely.
There had already been two recordings, so the first one was sent too:
My response was:
This is not a myocardial infarction.
Leads V4-V6 are something called "Benign T-wave Inversion".
Leads V1 and V2 look a lot like old MI (LV aneurysm), although that is unlikely given what we see in V4-V6.
I was not worried about the ST elevation.
Benign T-wave inversion looks just like this: ST elevation with high S-wave voltage in right precordial leads, and ST elevation concordant to a tall R-wave in V4, with a well formed J-wave.
I was then told the clinical history:
46 y.o. male without PMH who presents for weight loss for 1 week and back pain. Patient reports that he had noticed weight lost for a long time, but particularly in the last week.
An ECG was recorded because of a heart rate in the 120s.
He denied chest pain or dyspnea.
His labs had just returned consistent with hyperthyroidism.
The clinicians had been very worried about STEMI, and had appropriately performed a bedside echo.
Here is the parasternal short axis:
The first troponin returned below the level of detection. Remember that an undetectable troponin does NOT rule out STEMI or OMI (Our new terminology: OMI = Occlusion Myocardial Infarction -- See OMI Manifesto).
The low probability of OMI is due to:
1. Tachycardia (tachycardia is very unusual in ACS unless there is a second disorder or poor LV function. We will be presenting an abstract on this at SAEM. In our data, of ~2000 patients who had at least 2 troponins drawn within 24 hours, 877 had chest pain, EF greater than 50%, and SBP > 100. Of these, only 23 had a heart rate > 120 but none had type 1 MI.
2. The ECG morphology which, though meeting STEMI criteria, does not have the correct morphology for OMI.
3. The absence of wall motion abnormality, and hyperdynamic function.
4. The absence of chest pain
I advised that they do serial ECG and troponins, but neither Pathway A (cath lab activation) nor Pathway B [Pathway B" is a compromise between activating the cath lab ("Pathway A") and not activating. It is for emergent cardiologic evaluation for patients who might need emergent angiogram and PCI, but are complicated by an equivocal ECG or complicated medical problems.]
The next ECG was unchanged:
The patient ruled out for MI (all 4 serial troponins below the LoD) and was treated for hyperthyroidism.
See here for more examples of Benign T-wave Inversion, including a video presentation:
 |
| What do you think? |
I replied that precordial leads are misplaced and to record it again.
How did I know this? There are well formed R-waves in V1, but none in V2 and V3, then they return in V4. It is possible that there is focal infarction over V3 and V4, but very unlikely.
There had already been two recordings, so the first one was sent too:
 |
| Now the leads are in correct order. What do you think? There are 2mm STE in V2, 4mm in V3, and 2 mm in V4 |
My response was:
This is not a myocardial infarction.
Leads V4-V6 are something called "Benign T-wave Inversion".
Leads V1 and V2 look a lot like old MI (LV aneurysm), although that is unlikely given what we see in V4-V6.
I was not worried about the ST elevation.
Benign T-wave inversion looks just like this: ST elevation with high S-wave voltage in right precordial leads, and ST elevation concordant to a tall R-wave in V4, with a well formed J-wave.
I was then told the clinical history:
46 y.o. male without PMH who presents for weight loss for 1 week and back pain. Patient reports that he had noticed weight lost for a long time, but particularly in the last week.
An ECG was recorded because of a heart rate in the 120s.
He denied chest pain or dyspnea.
His labs had just returned consistent with hyperthyroidism.
The clinicians had been very worried about STEMI, and had appropriately performed a bedside echo.
Here is the parasternal short axis:
There is hyperdynamic function without any wall motion abnormality.
Here is the parasternal long axis:
Again, hyperdynamic without any wall motion abnormality.
The first troponin returned below the level of detection. Remember that an undetectable troponin does NOT rule out STEMI or OMI (Our new terminology: OMI = Occlusion Myocardial Infarction -- See OMI Manifesto).
The low probability of OMI is due to:
1. Tachycardia (tachycardia is very unusual in ACS unless there is a second disorder or poor LV function. We will be presenting an abstract on this at SAEM. In our data, of ~2000 patients who had at least 2 troponins drawn within 24 hours, 877 had chest pain, EF greater than 50%, and SBP > 100. Of these, only 23 had a heart rate > 120 but none had type 1 MI.
2. The ECG morphology which, though meeting STEMI criteria, does not have the correct morphology for OMI.
3. The absence of wall motion abnormality, and hyperdynamic function.
4. The absence of chest pain
I advised that they do serial ECG and troponins, but neither Pathway A (cath lab activation) nor Pathway B [Pathway B" is a compromise between activating the cath lab ("Pathway A") and not activating. It is for emergent cardiologic evaluation for patients who might need emergent angiogram and PCI, but are complicated by an equivocal ECG or complicated medical problems.]
The next ECG was unchanged:
The patient ruled out for MI (all 4 serial troponins below the LoD) and was treated for hyperthyroidism.
See here for more examples of Benign T-wave Inversion, including a video presentation:
Any signs of Hypercalcemia? Parathyroid issues noted?
ReplyDeleteAnother great post as always. Thanks for the many years of teaching. My practice as a Paramedic has benefited greatly.
Calcium normal
DeleteNICE case to illustrate a number of important points. I’d add the following thoughts to comments by Dr. Smith: i) In addition to illogical R wave progression — reasons we know the 1st ECG was recorded with erroneous precordial lead placement are that there is ALSO illogical P wave AND illogical ST-T wave progression. There is often at least some negativity to the P wave in leads V1, V2 — but really no reason why the P wave in this 1st ECG should be all positive in V1 — then biphasic in V2 — then all negative in V3 — and then all positive in subsequent leads. Similarly, the curved (ie, “frowny”-configuration) ST-T wave shape with ST elevation in lead V1 in the 1st ECG makes no sense given the very different slope of the ST segment in V2,V3 — before once again seeing coving with ST elevation in V4. The “take home” point — is that when such illogical progression is seen for P waves, QRS complexes AND ST-T waves — THINK of alternative lead placement possibilities. For example, if leads V1 and V3 would simply be swapped — progression of P waves, QRS complexes and ST-T waves instantly reverts to what should be expected. ii) Once chest leads are correctly placed (as in the 2nd ECG) — the principal findings include RAA + dramatically increased voltage for LVH. Voltage criteria for LVH are easily met in the limb leads (R wave amplitude clearly exceeds 20mm in ≥1 inferior lead) — as well as in the chest leads (Sum of deepest S in V1,V2 + tallest R in V5,V6 ~45mm {only ≥35mm is needed} — as well as showing tremendously increased S and R wave amplitudes in leads V3 and V4, respectively). Flipping over the QRST complex in leads V2 and V3 in this 2nd ECG (ie, performing a “mirror test”) — results in ST-T wave shape in V2,V3 that is the mirror image of LV “strain” (ie, anterior leads in patients with marked LVH often manifest this shape of ST-T wave abnormality — which strongly suggests LV “strain” rather than infarct-related ST elevation as the cause). iii) ST-T wave abnormalities in the 2nd ECG are generalized — rather than showing the more localized pattern characteristic of an OMI — and there really are no “reciprocal changes”. It is helpful to remember that the ST-T wave pattern seen in this 2nd ECG is characteristic of a type of repolarization variant in which there may be generalized ST segment coving with surprisingly deep T wave inversion. Often, there is more ST elevation in this pattern than is seen here. Perhaps the reason for this relatively limited amount of ST elevation (except for lead V3) — is that it has in part been cancelled out by the marked LVH that would otherwise have shown ST depression … THANKS again to Dr. Smith for posting this interesting case!
ReplyDeleteThanks, Ken!
DeleteNice clinical case. Thanks
ReplyDeleteNice clinical case. Thanks
ReplyDeleteSteve, would this EKG qualify to be tested using your BER vs STEMI equation? if not, why? (the LVH?).
ReplyDeleteso this is an EKG that "meets STEMI criteria". when shall i be brave enough, knowledgable and confident enough, NOT to call and arrange for cath lab, i wonder. an all the more important question in my shop, where the patient must be transferred to another distant institution.
thank you Steve ( and hello to Ken)
Tom,
DeleteMost easily, STEMI rarely has a heart rate this high unless there is poor stroke volume. As you can see from the bedside echo, the stroke volume is very high, with very high ejection fraction. Furthermore, once you've seen enough of these (partly by reading this blog), you'll recognize this morphology as a benign one.
Steve
Also, as for the formula: strictly speaking, because there are QS-waves, one should not use this formula, but rather the formula for differentiating old MI with persistent ST elevation (LV aneurysm) from acute STEMI. But this is clearly not LV aneurysm either. You could use both formulas and both would tell you that it is not STEMI: 1) BER: R-wave so tall in V4 that the formula would be negative 2) LVA: T/QRS ratios in all leads is low (T-wave is not tall, therefore not acute STEMI).
DeleteSee this post: http://hqmeded-ecg.blogspot.com/2017/04/st-elevation-and-qs-waves-in-patient.html
Can we say that the changes are repolarisation changes secondary to high voltage or may be calling it LVH with strain if there was no ECHO report available ?
ReplyDeleteI think it is just a benign variant, without acutal anatomic LVH
DeleteI’m not expert enough to assess LV wall dimensions from the bedside echo done in this case. I do have another opinion regarding the possibility of LVH based on the ECGs in this case — namely that in addition to dramatically increased QRS amplitude — the shape of the ST-T waves in correctly placed leads V1-V3 could be consistent with ST-T wave repolarization changes of LV “strain”. That said, ECG is far inferior to formal Echo study for assessment of true chamber enlargement — and this case is further complicated by: i) tachycardia; ii) hyperthyroidism with increased LV contractility; and iii) superimposed repolarization variant changes. As a result — I don’t think ( = my opinion) we are able to rule out true chamber enlargement from this single tracing. I’d LOVE to see results of formal Echo study on this patient to find out with more certainty.
Delete