Monday, September 24, 2018

Tachycardia and ST Elevation.

This Case was sent from Anonymous.

A middle-aged patient was sent to the ED with tachycardia. He denied any sensation of palpitations, but his heart rate was consistently 150 bpm. The other vitals were normal. He had JVD and swollen legs, but clear lungs and a normal room air oxygen saturation.

He denied all typical and atypical ischemic symptoms. He noted, however, that he had had marked fatigue starting about 5 days ago, but that he was actually feeling much better today.

The initial ECG:

The rhythm appeared to be atrial flutter, but also concerning were the ST segment elevations in I, aVL, V2, and V3, as well as ST depression in the reciprocal inferior leads.

But atrial flutter can alter the baseline such that there is only apparent STE or STD (see example cases below) 

Is this:
1) true STEMI (acute or subacute)?
2) PseudoSTEMI due to the underlying atrial flutter wave?
3) PseudoSTEMI due to old MI (persistent STE after previous anterior MI, also known as LV aneurysm morphology?

The physician's thoughts: This pattern is concerning for anterior wall OMI, specifically a proximal LAD lesion. There are Q waves in V1-V3, suggesting an old anterior MI, but the T waves in V2 and V3 are fairly tall, suggesting some degree of acute ischemia. Also, there are no T wave inversions which would suggest a subacute, evolved, or reperfused MI.

The patient, with an easy smile, again denied any symptoms.

Atrial flutter can mimic the ECG signs of an MI. (For example, see this case, this case, this case, these erroneous computer interpretations, and this case report

K. Wang makes this comment: "A great case. It's important, as you did, to point out, that atrial flutter waves can cause findings suggestive of STEMI. In this tracing, the answer is in the lead aVL. There, the beginning of the ST segment is higher than the top of the flutter wave in front of the QRS, proving that the ST segment is indeed elevated."

To clarify the ECG, the emergency physician administered IV metoprolol to slow the ventricular response. However, the patient became borderline hypotensive after this (although still completely symptom-free). A bedside echo was performed:
There is akinesis of the anterior wall, best seen on the parasternal short axis (PSSA) view.
So there is a myocardial infarction.
But is it old or new?
There is no evidence of aneurysm formation on this echo (the myocardial wall is not thin); therefore, it appears to be acute or subacute.

The cardiac catheterization team was activated. The blood pressure dropped precipitously while in the lab preparing for the angio, and the patient was electrically cardioverted. An occlusion of the proximal LAD was then found and intervened on.

The troponin obtained in the ED was almost 10 ng/mL, suggesting a subacute occlusion.

This was recorded next AM:
There are QS-waves with continued ST Elevation with large upright T-waves in V2 and V3

Smith comment:

Is this the so-called “left ventricular aneurysm” pattern? --LV aneurysm can be distinguished by the size of the T-wave, specifically the T/QRS ratio:

--LV aneurysm has a relatively small T-wave, often with some slight (shallow) inversion.

--Acute MI has a large upright T-wave, but may be inverted if reperfused (shallow in the case of Wellens' pattern A; deep in patthern B, which is a later evolution). However, Wellens' waves are preceded by R-waves, not by QS-waves.

LV aneurysm rule: One should especially suspect LV aneurysm, and use the rule, when there are QS-waves in any of V1-V4. A QS-wave means a single negative deflection, without any R-wave or with only a tiny r-wave.

Here is the rule:

If there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is acute MI. If less then 0.36, it is either subacute (over 6 hours) or old.(see references 1, 2). In this case, the T/QRS ratio is largest in V3 at 5/9 = 0.55.

If this were the presenting ECG, you would not want to say that those QS-waves are due to old MI with persistent ST Elevation (LV aneurysm morphology).

But now we are post-reperfusion, so what does the ECG tell us?
That there is persistent ischemia in spite of reperfusion.

This is a bad prognostic sign. The STE and hyperacute T-waves at this point could be either persistent ischemic or re-occlusion. If there had been intervening resolution on the ECG, it would represent re-occlusion. But in this case it was persistently elevated ST segments and hyperacute T-waves. This is typical of "no reflow," which is a result plugging of downstream small vessels by platelet-fibrin aggregates. Read about it here:

Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction (Lancet 1997)

[Alternative explanation for persistently upright T-waves: post-infarction pericarditis (which happens in transmural MI)].

T/QRS ratio to differentiate anterior STEMI from anterior LV aneurysm:

Case by Anonymous, continued

My personal M and M session:
If there is a similar “next time,” I may change my approach.

First, I deferred the echo too long. My initial reasoning was that this was just a rhythm problem, and that checking the Ejection Fraction at a rate of 150 was unreliable, and would be falsely low. Had I done the echo before the metoprolol, I likely would have felt more justified in considering cardioversion first!

Second, in retrospect, cardioversion would have been better than medications, both because his hemodynamics were precarious, and because it would have clarified the ECG interpretation. I delayed cardioversion because the patient looked “too good” for electrical therapy. Furthermore, the patient was likely in atrial flutter for greater than 48 hours, theoretically raising the risk of post-conversion CVA.

But sometimes ST changes will disappear with conversion of atrial flutter to NSR, and urgent angiography can be avoided. Or, in this case, the true ST segment changes will be revealed, and appropriate timing of angiography can be determined.

Smith comment:

I agree. Electrically cardiovert, then re-assess.

My Comment, by KEN GRAUER, MD (9/24/2018):
Excellent case for discussion. I’ll focus my comments on the 2 ECGs in this case, which for clarity I have put together in Figure-1. I’ll verbalize the thought process in my assessment, which led me to conclusions that mirror those detailed by Dr. Smith.
Figure-1: Comparison of the 2 tracings in this case. TOP — Initial ECG in the ED, obtained from this middle-aged patient with tachycardia. BOTTOM — ECG #2, obtained the following morning after cardioversion and cardiac catheterization (See text).
  • ECG #1 — shows a regular SVT (= SupraVentricular Tachycardiawith a narrow QRS complex, and a ventricular rate of ~150/minute. Sinus P waves are absent.
  • PEARL #1: It is helpful to keep in mind the differential diagnosis of a regular SVT rhythm in which sinus P waves are not clearly evident. For practical purposes, when the ventricular response is this fast, the differential diagnosis consists of 4 entities: iSinus tachycardia (which could still be present, if sinus P waves were hidden within the preceding ST-T wave); iiReentry SVT (such as AVNRT or AVRT); iiiAtrial Flutter with 2:1 AV conduction; and, ivAtrial Tachycardia with 2:1 AV conduction. Awareness of this short differential list greatly facilitates clinical decision-making.
  • The rhythm in ECG #1 is not sinus tachycardia. We know this is — because although there is atrial activity, the P wave in lead II is negative (slanted RED arrows). Unless there is lead misplacement or dextrocardia — a negative P wave in lead II excludes the possibility of a sinus mechanism.
  • PEARL #2: In my experience, AFlutter is by far the most commonly overlooked arrhythmia. The best way to avoid missing the diagnosis of AFlutter is to, “Think AFlutter until proven otherwise” — whenever you encounter a regular SVT at a rate close to ~150/minute, in which sinus P waves are not evident. If you regularly look for AFlutter in such cases — then you are far less likely to overlook it (See ECG Blog #40).
  • PEARL #3: You can virtually prove that the rhythm in ECG #1 is AFlutter even before slowing the rate by using CALIPERS. Set your calipers to exactly HALF the R-R interval — and see if you can precisely march out 2:1 AV conduction. If so — See in how many leads you are able to do so. We illustrate application of this technique in Figure-1. The non-sinus negative deflection before the QRS in lead II (slanted RED arrow) is perfectly equidistant from a similar-looking negative deflection right after the QRS (slanted PINK line).
  • The best leads to look for flutter waves with typical AFlutter are most often the inferior leads + leads aVR and V1 — and clear evidence of 2:1 AV conduction is seen in all these leads in this example (slanted PURPLE lines). Flutter waves are actually also seen in most of the remaining leads. Some cases of AFlutter only show flutter waves in 1 or 2 leads — but the more leads you clearly see 2:1 conduction in — the more confident of your diagnosis you can be without necessarily needing to slow the rate. NOTE: Reasons ECG #1 is unlikely to be ATach, are that this rhythm is much less common in a non-EP setting than AFlutter — and, that with 2:1 conduction, this would entail an atrial rate ~300/minute, which is clearly above the atrial rate usually seen with ATach.
As emphasized by Dr. Smith — AFlutter can alter the ECG baseline, making it extremely difficult to assess for acute ST-T wave changes. This is especially true when “typical” AFlutter is present, in which there are large amplitude flutter waves in the inferior leads, as well as in other leads. For this reason, I was not initially certain that the tall T waves with apparent ST elevation in the anterior leads of ECG #1 was indicative of an acute event. And, even though there are QS complexes in leads V1,V2 — with no more than tiny initial r waves in V3,V4 of ECG #1— these QRS morphologic changes do not always persist on repeat ECG under more controlled conditions after the rate has slowed.
  • PEARL #4: No matter how you might try to imagine “interference” from flutter waves affecting ST-T wave appearance in the anterior leads of ECG #1 — there is ≥2mm of ST segment elevation in lead aVL (LIGHT GREEN arrows, seen within the GREEN rectanglethat can not be explained away by flutter waves distorting the ST segment. That’s because we see NOTHING resembling flutter waves occurring at half-the-R-R interval distance away from the ST elevation in lead aVL (DARK GREEN arrows in this lead). In my experience — Lead aVis often a “magical lead” for providing the support needed to convince me that suspected ST elevation in equivocal cases is real.
  • Clinically — the case presented here is perfectly consistent with probable “silent MI” occurring about 5 days earlier (when this patient noted marked “fatigue”) — with persistent tachycardia and the likely large anterior STEMI accounting for gradual progression of right-sided heart failure (JVD, swollen legs noted). I took this as further support of my suspicion of recent acute STEMI.
PEARL #5: The best way to hone your Clinical ECG Interpretation skills — is to follow up on those cases about which you initially had questions on. Comparison of the initial ECG with ECG #2, obtained the next morning — provides us with an excellent opportunity to do this (Figure-1).
  • Note with reestablishment of sinus P waves in ECG #2 — that the double negative deflections in lead II (as well as in other leads) have disappeared.
  • Note in lead aVL similar shape and amount of ST elevation as we suspected from assessment of ECG #1 during AFlutter. Same is true (albeit to a lesser amount) in lead I.
  • Note the presence of “mirror image” reciprocal ST depression in each of the inferior leads in ECG #2. This was present in ECG #1 — though it was much more difficult to be certain this ST depression was real and not just superposition from AFlutter in the initial ECG.
  • Note similar QS complexes and poor R wave progression with persistent anterior ST elevation after conversion to sinus rhythm.
Our THANKS to Dr. Smith for presentation of this highly insightful case!


  1. Given that the atrial flutter had presumably been ongoing for several days, and the OMI/STEMI was fairly acute/subacute, is it likely that there was any causative relationship between the two, or do you suspect they were purely coincidental?

  2. These being coincidental is not very likely. I think it is more likely that ischemia (from an instable coronary plaque) triggered the atrial flutter, and this instable plaque then ruptured causing the STEMI. The other way around, which is less likely I think, would be an atrial flutter causing type 2 ischemia, and the tachycardia triggering the STEMI (such as physical activity and emotional stress can actually trigger an acute coronary event).

    1. @ Unknown — I agree. I think it more likely that the STEMI came first, and AFlutter was a result of the STEMI.


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