Written by Pendell Meyers, edits by Steve Smith
When practitioners are learning a new ECG concept for the first time, they very appropriately must go through a stage where they titrate their mind to the new finding, going through stages of over and under-recognizing. In my experience this is a normal phenomenon in all of medicine, and especially in ECG interpretation.
As I have recently been promoting recognition of hyperacute T waves among my group, I am getting more and more ECGs texted to me very appropriately asking “are these T-waves hyperacute?“
So let’s go over some hyperacute T-waves “ground rules”:
– There is no formal, universal definition of what constitutes a hyperacute T-wave. They could likely be defined as an elevation in the ratio of area under the ST-segment and T-wave compared to the area/size of the QRS complex. Although prior groups have described hyperacute T-waves simply as “tall and symmetric”(1), Smith et al showed that among patients with ischemic symptoms and at least 1mm STE in V2-V4, the absolute T-wave amplitude did not differ between patients with subtle LAD OMI and those with normal variant STE (“early repol”). When the T-waves in both groups were measured as a ratio of their preceding R-wave, those with subtle LAD OMI had proportionally larger T-waves than those with normal variant STE (T/R ratio = 0.7 for BER vs. 3.1 for LAD OMI) (2).
– However, in my experience this is not enough. There is also morphology to consider. Hyperacute T-waves are fatter than normal T-waves and usually more symmetric (these characteristics increase the area under the STT as well).
– Hyperacute T-waves are sometimes so impressive that they are diagnostic no matter the situation. Other times, you can only diagnose hyperacute T-waves by comparing the current questionable T-waves with a prior ECG.
– Because hyperacute T-waves are part of the OMI Progression, they localize to the affected distribution and have focal reciprocal findings as well.
– Like other OMI findings, they are usually maximal in the area of worst ischemia, and diminish radially outward in all directions from the OMI epicenter.
– What appear to be hyperacute T-waves may be reciprocal to reperfusion T-waves in an opposite distribution. If so, the pain will be resolving or resolved (e.g. posterior reperfusion T-waves, T-wave in aVL after reperfusion in III, T-wave in III after reperfusion in aVL).
Here are two such cases I received recently. What would you tell the team?
Case 1: “45 y/o pt with chest pain. No prior EKG. Is V3 hyperacute?”
|What do you think?
My response: “I do not think there is ECG evidence of occlusion. I would get serial ECGs to make sure there is no evolution or dynamic changes. Tell me more.”
Why don’t I think V3 is hyperacute?
Let’s pretend for a second that we only have lead V3 to look at. The T-wave in V3 is indeed large compared to its QRS. I do not think it has the “wide” or “fat” appearance that most hyperacute T-waves have. Nor does it look like hyperK. There is no terminal QRS distortion or pathologic Q-waves. Considered alone, I would not be able to tell you whether this represents a hyperacute T-wave or not. In the right context of surrounding leads and features, it could be.
Now let’s zoom out and consider it in context, because the context is what tells me that this T-wave is not hyperacute.
If V3 is indeed showing evidence of OMI, then its next-door neighbors should usually (but not always) help to corroborate this claim. As you get better at ECG’s, you really can’t help but personify them in your mind. Dr. Smith always says that “ECGs are like faces, you just have to recognize them.”
Consider this analogy: You get a report from a single house that there might be an earthquake happening in that area. You call the house next door and they are acting normally, and they have no idea what you’re talking about. The story is not corroborated by the next-door neighbor. Something doesn’t fit.
V2 has small voltage and a relatively large T-wave, which again could theoretically be hyperacute out of context.
V4, however, is the model of what all V4’s strive to be: tall, dark, and handsome R-wave, followed by an ST segment perfectly at baseline, with a perfectly proportional T-wave following. V4 disagrees with the idea of V3 being hyperacute. The next door neighbor has no idea what you’re talking about.
There are no pathologic Q-waves, no terminal QRS distortion, no reciprocal changes, and no concerning ST morphology findings on the ECG.
Out of curiosity I ran it through the formula:
|The closer the score is to the derived cutpoint of 18.2 (e.g. greater than 17.7 or less than 18.7) the more likely it is to represent a false negative or false positive.
So this is just barely positive!
I just did not think this was OMI based on ECG. So I told the team this, but reminded them that the ECG is not the only data point in the decision to perform emergent cath. The patient apparently did not look ill, limited US during pain was apparently unremarkable, and there was no hemodynamic or electrical instability.
They got several serial ECGs, all of which were unchanged. At some point the chest pain resolved.
Three troponins were negative.
Finally, a CT coronary angiogram (CTCA) was performed which showed normal coronaries.
The patient was appropriately discharged with chest pain of unknown cause.
Case 2: “40 year old man presenting with crushing chest pain described as ‘like my other heart attacks’, also missed dialysis. Is V3 hyperacute?”
|What do you think?
My response: “I do not think there are hyperacute T-waves. I see no evidence of occlusion, but remember the ECG is not the only reason to activate. Would get serial ECGs and observe for evolution, assuming nothing else is concerning. Possible mild hyperK changes, would need baseline.”
They immediately texted me back, saying “Does his troponin T of 1.21 change your interpretation?”
Generally, this troponin alone in the context of crushing chest pain is indeed an indication for the cath lab, no matter what the ECG shows.
My response: “Not about the ECG. But it should factor into the case as a whole. Where’s the baseline? What’s the story?”
Why do I think V3 isn’t hyperacute?
Considered in isolation, V3 does have a large, tall T-wave which is big for its QRS complex. Like the last case, it is not fat or broad. By itself, it would be concerning but not diagnostic for a hyperacute T-wave.
So look next door: V2 has very high voltage followed by expected small STE and positive T-wave which is actually very small for such a large QRS complex. If V3 represented a hyperacute T-wave, V2 should at least hint that its T-wave is at least marginally concerning. But instead V2 is perfectly normal for its QRS.
V2 does not corroborate V3. Neither does V4.
Additionally, I think this represents a common mistake which happens most often in the transition lead. The “transition lead” is the precordial lead in which the QRS transitions from mostly negative QRS components to mostly positive. In this case, V2 is predominantly negative, and V4 is predominantly positive. Therefore V3 is the transition lead, and is almost isoelectric. Both V2 and V4 have considerable voltage.
You may ask “so where does all this voltage go between V2 and V4?”, “why does V3 have such a small QRS then?” The way I answer this is to say that the voltage in V3 is “folded up” inside the QRS complex. This is sometimes the case in the transition lead, as the QRS is often isoelectric and has multiple conflicting component vectors. Most often, the transition lead simply has the same overall QRS voltage but with equal R and S components. Sometimes, however, the transition lead produces what appears to be a small QRS complex between two large high voltage QRS complexes. I think of this as the voltage being “folded up” into the transition lead QRS complex. This helps me understand why the T-wave appears so large in this lead.
However, I am unable to find any literature that supports or denies this assertion.
You may also ask about the negative T-wave in aVL, wondering if this is a clue to inferior OMI. No, because the inferior leads do not show evidence of OMI, and the QRS in aVL is also negative, so it is not unexpected to have a negative T-wave at baseline.
Here is the baseline ECG:
|There are some differences, including lower voltage. The differences do not make the current ECG more concerning in my opinion.
Here is the repeat ECG:
|I think there is no significant change.
Another repeat with no significant change:
I looked back in the patient’s chart and found out that he had multiple similar visits, each time with missed dialysis followed by crushing chest pain and highly elevated troponins, always with similar ECGs. The first time, the cath lab was activated and the patient had normal coronaries, with absolutely no CAD. Each time, his troponin T elevated higher than 1.0 ng/mL with rise and fall diagnostic of MI, but obviously not of Occlusion MI. This is type 2 MI likely due to a variety of factors.
Warning: This is a bizarre case. It is highly unusual for a conventional troponin T level to be this high during an episode of crushing chest pain without ACS. 15% of patients with renal dysfunction have an elevated baseline troponin, but usually no more than 5x upper reference limit, sometimes up to 15x, but rarely higher (3). Conventional Troponin T of 1.0 ng/mL or greater is much more common in the setting of Occlusion MI than in Non-Occlusion MI. Without the history of the previous identical visits with completely negative cath recently, it would be completely appropriate to activate the cath lab based on crushing chest pain and such a highly elevated troponin, even in the absence of ECG findings.
The team found this information, and given no change in serial ECGs with this history, they admitted the patient for emergent dialysis. After dialysis, his symptoms resolved. The troponin rose and fell, peaked at 1.64 ng/mL. His baseline trop is unknown. No cath was performed.
Warning: I am not saying that a hyperacute T-wave must always have corroborating evidence in both neighboring leads. I am simply saying that checking both adjacent leads is a helpful step in determining whether findings in one lead are indicative of OMI when there are no other concerning or corroborating features. Here are some cases you might use to tell me I’m wrong because the hyperacute T-waves seem to have some surrounding leads which might not appear concerning to everyone:
In both cases, however, there are other concerning features even if one of the neighboring leads to the hyperacute T-waves is relatively normal.
Only experience and time will make you better at distinguishing hyperacute T-waves from normal variants. See these many examples for comparison:
10 Cases of Anterior Hyperacute T-waves in V2-V3
10 Cases of Anterior/Lateral Hyperacute T-waves in V4-V6
10 Cases of Inferior Hyperacute T-waves
Missed hyperacute T-waves followed by death
Hyperacute T-waves that never manifested STE despite serial ECGs with total anterior wall infarction
30 year old with hyperacute T-waves diagnosed prehospital
Missed hyperacute T-waves followed by cardiac arrest during discharge
Hyperacute T-waves called “normal” by computer
Another prehospital hyperacute T-wave case
Hyperacute T-waves have no formal definition, and sometimes require comparison with prior ECGs and repeat ECGs.
Interrogate the neighboring leads to see if they corroborate a questionable finding.
The skill to detect subtle Occlusion MI must be developed simultaneously with the ability to weed out the mimics. We are trying to deliver immediate reperfusion to those with OMI and prevent unnecessary harm to those without.
1) Nikus K, Pahlm O, Wagner G, et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology. J Electrocardiol 2010;43:91-103.
2) Smith et al. Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation myocardial infarction. Annals of Emergency Medicine 2012.
3) Vasudevan et al. Renal function and scaled troponin in patients presenting to the Emergency Department with symptoms of myocardial infarction. Am J Nephrol 2017;45:304-309.
K. Wang’s comments:
Good cases and discussions of tall T waves in the precordial leads. Tall T waves in the precordial leads should make one think of three conditions, namely, hyperkalemia, hyperacute ischemia and normal variant. Typical examples of these three are illustrated in the “Atlas of Electrocardiography by K. Wang
“, page 171.
As can be clearly appreciated, they look different. The first two are symmetric while the normal variant is not (upstroke takes more time than the downstroke). In hyperacute ischemia. the upstroke is a straight line ,and, so is the downstroke, while they are “tented’ in hyperkalemia. Of course, I have picked typical examples here. Unfortunately not all cases are typical and some fall in the borderline, making us agonize. But that’s life! Still, one has to know what typical cases look like to start the discussion.
The beauty of Dr. Smith’s ECG blog is that it is based on his years of clinical experience backed up by coronary angiography and patient outcome.