"It isn't a STEMI," so cath lab refusal (again). Were they right?

Sent by Anonymous, written by Pendell Meyers

An elderly female called EMS for acute epigastric pain. EMS arrived and recorded this ECG on the way to the hospital:

This case was sent to me with only the details above, and my response was: 

"It's posterolateral (and probably also inferior) OMI until proven otherwise. I'd also give a little calcium because it's slow, wide, and a couple leads have almost pointy Ts. But I don't really think it's hyperK. This one is OMI. Either LCX or RCA, or perhaps an Obtuse Marginal that supplies those regions."

Interpretation: There is an absence of sinus activity, including an absence of retrograde P waves. The rhythm is probably a junctional escape at a rate of approximately 45, with RBBB and likely also LAFB (given the leftward axis despite RBBB). Alternatively, it could be a posterior fascicular escape. There is STD in V2-V5 that is maximal in V2 and V3. This STD is excessively discordant in V2, and concordant in V3. The inferior leads show Q waves with STE in lead III, and there is some slight reciprocal STD in I and aVL. Interestingly, many of the T waves have a slightly peaked appearance. Along with bradycardia and conduction block, this would be alarming for potential hyperkalemia, which of course can also cause OMI mimics. We have shown several cases on this blog that appear to have both OMI and severe hyperkalemia.

Additionally, both 1) no spontaneous sinus activity (sinus arrest or extreme sinus brady) and 2) no retrograde activity, which implies AV block as well

Cardiology was summoned immediately to bedside but they thought that this ECG "isn't a STEMI" and refused to take the patient to the lab. 

The initial troponin T returned highly elevated at 4.04 ng/mL. The potassium was 4.1 mEq/L. Cardiology was recalled to bedside to reevaluate.

Smith comment: When Pendell texted this to me, I thought it was both hyperkalemia and inferior posterior OMI.  V4 and V5 especially have the appearance of hyperK.  This just goes to show that there are always false positives and false negatives.

Another ECG was recorded:

These are almost certainly posterior leads, though they were not labelled as such (V4-V6 are really V7-V9 on the posterior thorax). 
How do we know? We can tell this because of the very low QRS amplitude and the Q-waves.  The slight ST elevation is diagnostic of posterior STEMI, which in posterior leads only requires 0.5 mm in just one lead to meet "criteria."

There are possible atrial waves but it is not definitive with this low quality ECG. If the possible atrial waves are real, it could be sinus bradycardia with 2:1 AV block. Otherwise, this would be complete heart block with junctional escape. The rate is approximately 30 bpm. Apparently the patient was mentating and had a normal blood pressure with this, and did not require pacing at that moment.

We do not recommend posterior leads in this situation because they are unnecessary (the initial ECG is diagnostic of posterior MI) but they might be falsely negative and dissuade you from your diagnosis. 

Why are posterior leads falsely negative?  2 reasons: 
1) they are often recorded at a later time, after the artery has reperfused.  It is easy to recognize this if you are aware: V1-V3 will still be recorded and visible, and the STD in these leads will be gone.
2) the voltage of posterior leads may be very small because the signal needs to traverse the lungs.


The patient was taken to cath where a 100% (TIMI 0) LCX occlusion was found and stented. No further troponins were ordered.

The patient survived so far.

Learning Points:

RBBB should have a small, proportional amount of appropriately discordant STD and T wave inversion in leads with large R' wave (usually just V1 and V2). At some point, STD in these leads becomes out of proportion. This case is an excellent example of excessively discordant STD in RBBB, maximal in V2-V4, which signifies posterior OMI in RBBB.

Make sure to keep hyperkalemia on the differential for any sick patient with bradycardia, wide QRS, AV blocks, and bizarre morphology. It would have been an excellent choice to give this patient IV calcium on arrival to see if the ECG responded, while also treating for OMI simultaneously.


MY Comment by KEN GRAUER, MD (9/28/2020):


Superb interpretation of the presenting ECG in this case by Dr. Meyers!

  • As per Dr. Meyers — the combination of QRS widening + bradycardia + lack of sinus P waves should immediately suggest the possibility of Hyperkalemia — especially since T waves in no less than 8/12 leads (ie, in leads I,II,aVL,aVF; and in V3-thru-V6) in the initial ECG look more-peaked-than-they-normally-should-be. For this reason — Dr. Meyers appropriately suggests that empiric Calcium would be a reasonable option in this circumstance, even before knowing the serum K+ level.
  • NOTE — I would bet that No One who regularly follows Dr. Smith’s ECG Blog has trouble recognizing hyperkalemia when all of the typical findings are present. That said, many of our patients simply “don’t read the textbook” — and recognition of hyperkalemia becomes much more challenging when T wave peaking isn’t obvious (ie, when T waves aren’t so pointed with such a narrow base — or, when other abnormalities such as RBBB are present). For this reason — I thought it worthwhile to review some less appreciated ways in which hyperkalemia may present.

Regarding HyperKalemia & Brady Rhythms: We have previously discussed on numerous occasions in Dr. Smith’s ECG Blog, the multiple ECG manifestations of various degrees of HyperKalemia. Among these:

  • Review of sequential ECG changes of Hyperkalemia — in My Comment at the bottom of the January 26, 2020 post.
  • And, relevant to the bradycardia and lack of P waves in today’s tracing — My review of the mechanism for the various ECG changes (My Comment in the July 3, 2020 post) — which I restate here: The characteristic T wave peaking of hyperkalemia is seen early in the process — due to an acceleration by elevated K+ levels of terminal repolarization. With more severe K+ elevation — there is depression of conduction between adjacent cardiac cells, eventually with depression of SA and AV nodal conduction. This may result in a series of conduction defects, including PR and QRS interval prolongation — frontal plane axis shift — fascicular and/or bundle branch block (including interventricular conduction defects— and/or AV block with escape beats and rhythms. Ultimately, QRS widening may lead to a sine-wave appearance (fusion of the widened QRS with the ST-T wave — such that distinction between the two is no longer possible). If this severe hyperkalemia remains untreated — VT, VFib or asystole are likely to result as the terminal event.
  • As serum K+ increases — P wave amplitude decreases. Ultimately, P waves may disappear. This is because atrial myocytes are exquisitely sensitive to the extracellular effects of hyperkalemia (much more so than the SA node, AV node, the His, and ventricles). As a result — despite lack of atrial contraction (ie, loss of P waves on ECG) — there may still be transmission of the electrical signal from the SA node over the conduction system and to the ventricles. Thus, rather than a junctional rhythm or fascicular escape rhythm — a bradycardic rhythm without visible P waves in severe hyperkalemia may be a Sino-Ventricular Rhythm (in which despite lack of P waves on ECG — the rhythm IS still initiated in the SA node, with electrical transmission through to the ventricles). But because P waves disappear and the QRS is often wide with a hyperkalemic sino-ventricular rhythm — it is EASY to mistake this rhythm as either AIVR (Accelerated IdioVentricular Rhythm) or VT.
  • BOTTOM Line: The bradycardia, altered P wave activity and the different forms of widened QRS morphologies may make for multiple potential ECG manifestations when there is severe hyperkalemia. The only way to prevent overlooking the diagnosis in some of these patients — is to always consider the possibility of HyperKalemia whenever presented with a tracing such as the one that was seen in today’s case.

— BUT — Serum K+ in this case turned out to be normalTherefore — the ST-T wave appearance in today’s case is not the result of hyperkalemia.

QUESTION: If I were to show you the ECG that appears in Figure-1 — Would you have any doubt that this is an acute STEMI?

  • HINT: The answer is “No”.

Figure-1: How would YOU interpret this tracing?

MY Thoughts on ECG #1: In the context of the obvious acute STEMI-like ST elevation in leads V1, V2 and V3 of Figure-1 — supportive ECG findings that we see in other leads should become unmistakably obvious:

  • There is definite ST elevation in lead III — with reciprocal ST depression in high lateral leads I and aVL. These high lateral leads also manifest suspicious-looking terminal T wave positivity of surprisingly high amplitude.
  • The T wave in lead II is obviously hyperacute (much more “voluminous” than-it-should-be, given modest depth of the S wave in this lead).
  • In this context — the T wave in lead aVF is probably also hyperacute (given small depth of the S in this lead).
  • All 3 of the lateral chest leads (leads V4,5,6) manifest clearly hyperacute T waves given modest QRS amplitude of the complexes in each of these leads. In addition, ST segments leading up to these hyperacute T waves are abnormal (depressed in V4; straightened in V5; and straightened with a rising takeoff in V6).

COMMENT: Despite the above described obvious abnormalities in 11/12 leads (actually in all 12 leads if you count the ST elevation in aVR) — in this elderly patient with new-onset potential chest pain “equivalent”symptoms — this case presents yet one more instance of the cardiology team stating, “Not a STEMI — therefore NO indication for acute cath.” I have to admit that I just do not understand this refusal ... (We’ve published many similar examples of this type of oversight — the most recent of which in our September 21, 2020 post).

CONFESSION: The 12-lead tracing I show above in Figure-1 was altered by me. I simply inverted the 3 leads within the RED rectangle (to project the mirror-image of leads V1, V2 and V3).

  • I show the actual initial ECG in today's case in Figure-2 — to which I’ve added the inverted (mirror-image) view of leads V1, V2 and V3 to the right of ECG #1.
  • As I’ve described in many prior posts on Dr. Smith's ECG Blog (See especially My Comment from Sept. 21, 2020) — the Mirror Test is no more than a simple visual aid that inverts anterior leads, thereby facilitating recognition of the shape of an acute posterior MI. It is based on the principle that the mirror-image of anterior leads provides insight into the appearance of ongoing electrical activity in the posterior wall. With a little practice — you’ll find posterior leads are rarely (if ever) needed — because use of the Mirror-Test allows instant recognition of virtually all cases when there is acute posterior MI.
  • NOTE: Regardless of whether you call the ST-T wave appearance in the anterior leads of ECG #1 (in Figure-2) a “STEMI-equivalent” (since technically there isn’t ST “elevation” ) or simply an OMI — this pattern in a patient with new symptoms reliably identifies acute Occlusion-based MI.
  • Final POINTS: The shape of the ST-T waves in leads V2 and V3 of ECG #1 in Figure-2 is clearly abnormal! Note how much J-point ST depression there is for the ST segment in lead V2. This is not seen with simple RBBB. The 2 mm of J-point ST depression with shelf-like straightening of the ST segment in lead V3 is also not a “normal accompaniment” of simple RBBB. Some ST-T wave depression is expected with uncomplicated RBBB — but generally this should be maximal in lead V1 (and not increasing as we move laterally toward leads V2, V3, as we see in Figure-2).

Figure-2: The initial ECG in this case, with the mirror-image of leads V1, V2 and V3 placed to right of ECG #1 (See text).

Source: hqmeded ecg

"It isn't a STEMI," so cath lab refusal (again). Were they right?