Conclusion to 43 Year Old Female – Chest Discomfort After Eating

This is the conclusion to our case from last Saturday. I suggest reviewing the original case presentation before diving into the discussion here.

A 43-year-old female presents feeling like there’s a knot behind her sternum. It began suddenly just after eating lunch. This is her initial ECG:

1164 - ECG 01

There is apparent ST-elevation in leads V1–V3. The question remains, however, whether this ECG shows a STEMI or just early repolarization. Let’s look at the factors affecting our diagnosis:


The Story

At first glance this patient’s story doesn’t seem too impressive. It sounds like she might have a food bolus obstructing her esophagus or maybe even some esophageal spasm or heartburn, but it’s important to remember that our first priority in emergency medicine is to rule-out badness. In this case the most concerning diagnosis in play is acute MI.

Looking at her symptoms objectively: she experienced a sudden onset of retrosternal chest pain that radiates to her left scapula. The pain is constant with associated nausea.

In the absence of findings highly diagnostic of a food bolus (i.e. inability to swallow saliva or water), it doesn’t matter that her vitals are normal and she isn’t short-of-breath, diaphoretic, vomiting, experiencing arm or jaw pain, or any of the other secondary features we associate with an acute MI. The symptoms that are present should have us considering MI until proven otherwise—especially in light of her borderline ECG.



So we’re going to manage this patient as a possible AMI from a prehospital standpoint. The question now is whether she is experiencing an ST-elevation myocardial infarction (STEMI)—requiring immediate reperfusion—or if the ECG is non-diagnostic and she can be further evaluated in the ED.

Well, I can tell you that it is indeed a STEMI. The reasons?

  • There’s too much ST-elevation in V1–V3 for a 43yo woman.
  • The T-waves in V1 and V2 are slightly too tall.
  • The take-off of the ST-segment in V2 is slightly to steep.
  • There are clear reciprocal changes.

While the first three findings work together to increase our suspicion of STEMI, it is the last one that seals the diagnosis. That will be the most important aspect of our discussion but first…

The Elevation

Using the PR-segment as baseline and measuring at the J-point, there is 1.5 mm of elevation in V1, 1.5 mm of elevation in V2, and 1.1 mm of elevation in V3. According to the ECG criteria cited in the Third Universal Definition of Myocardial Infarction (which is used by the AHA in their STEMI guidelines), this ECG would just barely qualify as a STEMI with 0.15 mV in V1 (> 0.10 mV needed) and 0.15 mV in V2 (= 0.15 mV needed). V3 would not meet STEMI criteria with 0.11 mV (< 0.15 mV needed).

1164 - ECG 01 (V1-V3 ST measure)

3rd Universal Definition MI - STE Criteria

While it’s nice that the patient meets the formal criteria, ECG’s that fall close to the values above tend to produce a lot of false-positives and false-negatives. That doesn’t instill too much confidence if we’re more concerned with making an accurate diagnosis than simply meeting the minimum standard set by the guidelines.

Anyone who has been following the blog should realize that we don’t often invoke millimeter criteria in our discussions. In fact, except when I’m using Dr. Smith’s formula to differentiate STEMI from early repolarization, I haven’t felt the need to measure the actual amount of ST-elevation on an ECG in a few years. The whole reason I even mention it in this discussion is that, while there is measurable ST-elevation, the actual values don’t offer us much guidance. Even if you’re going to use the guidelines to define a “STEMI” in your region, in a case like this you’ll probably want to have more to go on than a measurement that just barely meets the formal (and arbitrary) cutoff.

Much more important is the morphology of the ST-segments and T-waves and the presence of reciprocal changes.

Reciprocal Changes

So about those reciprocal changes…

They are best seen in leads I, aVL, V5, and V6.

1164 - 48yo F - CP x 30 min 01 (reciprocals)

  • Lead I: There is about 1 mm of horizontal ST-depression. This is concerning but not a slam-dunk.
  • aVL: There is about 0.5 mm of ST-depression with an inverted T-wave. This is also worrisome but still non-diagnostic.
  • V5: There is about 0.5 mm of ST-depression. This is slightly less concerning but significant in light of the other findings.
  • V6: More important than the amount of ST-depression present, the morphology of the ST/T-wave here is markedly abnormal. This finding is certainly ischemic in nature here and, combined with the borderline ST-elevation in the right-precordial leads, confirms the diagnosis of STEMI.

In most situations you shouldn’t see an ST-segment that slopes downward into an upright T-wave like we do in V6 (though there are certainly exceptions; some cases of LVH with subtle strain come to mind). It is usually an ischemic finding. Sometimes that ischemia is just due to increased demand from an elevated heart rate, but that’s still ischemia and worth noting.

As a result, there are times this morphology might be non-diagnostic or of little concern, such as when it is due to subendocardial ischemia in a septic patient or even an unusual normal-variant.

0832 - 62yo F

The ST-depression we see here could be ischemic but there are no signs to suggest it is reciprocal to a STEMI. This patient ended up ruling-out for MI.

In the ECG above (from a different case), we see a similar morphology in V3–V6. It turns out, however, the patient ruled-out for acute MI (troponin-I 0.01 ng/mL x 3 (ref <= 0.04 ng/mL)). This pattern was also nearly identical to her baseline tracing.

The big difference from our case, however, is the lack of ST-elevation anywhere.

When coupled with borderline ST-elevation our point-of-view changes from, “Maybe that’s just a little ischemia; let’s keep an eye on it,” to, “Those are reciprocal changes—Open the cath lab!”

0183 - 01

Here’s a more obvious anterior STEMI with that same reciprocal down-up ST/T morphology in V5, V5, II, III, and aVF.

1209 - 01

Here’s another subtle STEMI (LCx culprit) with the same reciprocal morphology in V3–V6 and II, III, and aVF.

1393 - 09

This is an exceptionally subtle MI with that down-up reciprocal morphology visible in leads III and aVF.

0054 - 01a

This is very similar to the last ECG except for the frankly inverted T-wave in III, but there’s still that down-up pattern in aVF.

0827 - 01

Another subtle anterior STEMI. This time the down-up pattern is only seen in lead III. For more from this specific case check out our write-up here.


What if there aren’t reciprocal changes?

Well that just makes your job harder. Unfortunately lack of reciprocal changes, while a bit reassuring, in no way rules out a STEMI. If you’re worried about anterior STEMI but don’t see reciprocal changes, you should still be worried.

0685 - 02

Early (hyperacute) anterior STEMI. If an EKG this impressive shows no reciprocal changes you can imagine how tough it can be to identify a more subtle anterior STEMI without reciprocals.

0836 - 01

Subacute anterior STEMI with a culprit in the mid-LAD and no reciprocal changes visible.

0700 - 03

STEMI showing near-global ST-elevation and no reciprocal changes.

Dr. Smith's ECG Blog

Proven anterior STEMI in a 30-something male patient showing no reciprocal changes. ECG is reproduced from Dr. Smith’s ECG Blog. Click image for source.



Going back to our initial case; the patient first stopped in the emergency department where she had some labs drawn and a chest X-ray performed.

Her initial troponin-I on a current-generation assay (in the U.S.; not high-sensitivity) came back undetectable at < 0.01 ng/mL (ref <= 0.04 ng/mL). Thankfully an astute emergency physician recognized the significance of the patient’s ECG and activated the cath lab before that value returned. Had they waited for the troponin they would have been falsely re-assured as it was still very early in the patient’s MI and the level simply had not had time to appreciably rise.

I doubt this patient would have gone to cath if they knew her initial troponin was “negative.”

Cath revealed an acute lesion in the proximal LAD that was stented to good result.


Addendum: Dr. Smith’s Formula

Earlier in this post I mentioned Dr. Smith’s formula for differentiating anterior STEMI from early repolarization. I love the formula and have found it to be highly accurate but there’s a reason I didn’t use it here:

We aren’t allowed to!

You cannot apply the formula to ECG’s with possible reciprocal ST-depression (along with several other exclusions).

While it is tempting to use the formula because the abnormalities here are not impressive, the presence of any reciprocal changes precludes its use. Had we tried to use it (with values of 2.0 mm, 375 ms, 13.5 mm), it would have given us an output of 20.1. This is much less than the cutoff of 23.4 and would be falsely reassuring that the patient wasn’t experiencing a STEMI.

Dr. Smith’s formula is very, very useful (though not perfect), but it has to be used properly to work.

Colchicine in acute gout: high-dose or low-dose or no-dose?

003206 Colchicine, 0.6mg, 1,000 Tablets per Bottle McGuffMedical.com3.5 out of 5 stars

Does Colchicine Improve Pain in an Acute Gout Flare? Turner J, Cooper D. Ann Emerg Med 2015 sep;66:260-1.


The 7th edition of Tintinalli’s Emergency Medicine (2011) has this to say about using colchicine to treat gout:

Oral colchicine is typically administered in a dose of 0.6 milligrams/h until intolerable side effects (vomiting or diarrhea) or efficacy ensues.

This “typical” dosing schedule goes back decades, and even when I was a medical student who didn’t know an Ewald tube from an Ewok it never made sense to me. The instructions might as well have been “Take this until you’re better or you find you’re shitting and puking your guts out.”

And this dosing made even less sense when I realized that the “intolerable side effects” were actually symptoms of colchicine toxicity which can be — and not infrequently is — life-treatening.

Is there any evidence on this issue? This short synopsis summarizes a recent article updating the 2006 Cochrane review of the topic. The authors of that review found only 2 randomized controlled trials that met inclusion criteria. One trial (43 patients) gave 1 mg colchicine orally, then 0.5 mg  every 2 hours until complete relief or toxicity, or placebo. The second study (575 patients) compared placebo v. high-dose colchicine (4.8 mg over 6 hours) v. low-dose colchicine (1.2 mg then 0.6 mg one hour later.)

The take-home message:

“Low-quality evidence suggests that both high- and low-dose colchicine decreases [sic] pain in acute gout flares; however, high-dose regimens are associated with more frequent adverse effects.”

Note that there were adverse effects associated with use of the low-dose regimen. (For that matter, there were also adverse effects in the placebo groups.) This synopsis gives no indication of the nature or severity of these effects. Unfortunately, there are no trials comparing colchicine to other modalities such as non-steriodal anti-inflammatory agents in these patients.

Also remember that renal insufficiency is a contraindication to the use of colchicine, especially in high doses.

To read my Emergency Medicine News column on colchicine toxicity, click here.

Related posts:

Colchicine: tips for avoiding fatal in-hospital toxicity

Colchicine: be afraid, be very afraid

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