Conclusion to 59 Year Old Male: Unwell

This is the conclusion to our latest case, 59 Year Old Male: Unwell. I suggest starting there and reviewing the scenario before diving into this discussion.

I was glad to see our latest case generated quite a bit of debate. This is a difficult tracing coupled with an equally difficult clinical scenario, so it wasn’t surprising there were a variety of treatment plans. What’s less debatable, however, is the interpretation of the first two ECG’s:

Initial ECG

Fig. 1. Initial ECG showing STEMI with rapid AF and a bifascicular block. Click to enlarge.

  • Atrial fibrillation with rapid ventricular response
  • Right bundle branch block (RBBB) + left anterior fascicular block (LAFB) [Bifascicular block]
  • Acute STEMI due to a LMCA or proximal LAD culprit

I’m going to have to put together a second post where we actually discuss the management of this patient, but this article is going to focus purely on the electrocardiograms. There’s a lot of fine details we can (and will) pick apart, but the three points above should be spot-diagnoses in a case like this.

For most providers they aren’t.

And it actually has very little to do with individual skill or experience. Looking at the comments when we first posted the case, a lot of folks—including those who usually nail even our toughest cases—got distracted by the “wide and fast” rhythm. Unlike most of our other cases where we encourage a step-by-step analysis, this particular situation is one where strict pattern recognition may initially serve you better.

Once you train yourself to recognize the underlying pattern, however, the above diagnoses should come to you like instinct. After initially stabilizing the patient you can take a second look at the ECG’s to tease out more details and consider whether you might be might be dealing with a STEMI mimic (hyperkalemia comes to mind)—some would term that “System II” thinking—but your goal at the end of this article should be to recognize the three major findings listed above within seconds.

Rather than going step-by-step starting with the rate, rhythm, axis, etc… as we are all trained, I’m going to discuss it in the order my brain actually processed the images the first time I saw them.


The Pattern

Let’s start by running through the pattern that initial ECG brought to mind the moment I saw it: RBBB, LAFB, and massive antero-lateral STEMI.

ECG reproduced from this case at Dr. Smith's ECG Blog.

Fig. 2. Sinus tach, RBBB, LAFB, and massive STEMI. ECG reproduced from this case at Dr. Smith’s ECG Blog.

01 - 85yo M

Fig. 3. Uncertain irregular rhythm with RBBB, LAFB, and massive STEMI. ECG reproduced from this case on our blog.

Sinus tach (with extopy), RBBB, LAFB, and massive STEMI. Image reproduced from Figure 1 of the Invasive Cardiology article linked here.

Fig. 4. Sinus tach (with extopy), RBBB, LAFB, and massive STEMI. Image reproduced from Figure 1 of the Invasive Cardiology article linked here.

Image reproduced from the NEJM article linked here.

Fig. 5. Uncertain regular rhythm with RBBB, LAFB, and massive STEMI. Image reproduced from the NEJM article linked here.

Image reproduced from Figure 2 of the Journal of Electrocardiology article linked here.5

Fig. 6. Sinus tach with RBBB, LAFB, and massive STEMI. Image reproduced from Figure 2 of the Journal of Electrocardiology article linked here.

In all of these cases the patients experienced large STEMI’s due to a culprit in the LMCA or proximal LAD. Commit these tracings to memory.


Is There Really A STEMI?

While the pattern seems to fit, it’s still hard to pick out whether we’re actually looking at true ST-elevation on the initial ECG.

To be honest, the first thing I look at on almost any EKG is the ST-segments. As Willie Sutton [allegedly] said, “…that’s where the money is.” It’s electrocardiographic heresy to admit you don’t perform a step-wise analysis starting with the rate, rhythm, axis, etc… (though anyone in-training should and I still do when practicing), but my gut doesn’t care that the complexes are wide, fast, and irregular—if I’m not immediately cardioverting the patient or pushing calcium (another discussion), my next priority is identifying STEMI.

I chose to share the messy ECG at the top of the page several hours before updating the case with a cleaner tracing for a very specific reason: though you cannot accurately assess the precordial leads on that first ECG, it’s still diagnostic for STEMI.

Keeping with our policy of going right for the money, rather than trying to dissect out the J-points in all the leads or wading through the precordial artifact, let’s just focus on the two leads with the most prominent ST-deviations: III and aVL.

ST-elevation in aVL with marked ST-depression in III.

Fig. 7. ST-elevation in aVL with marked ST-depression in III.

Now those two leads slightly deceiving. Given only Figure 7 you might think the QRS duration is only 90 ms instead of its actual measurement of something like 160 ms (more on that later), but that’s okay. I usually don’t condone self-deception or sloppy interpretations but in this case it doesn’t really matter whether the QRS is 90 or 160 ms wide; there is significant ST-elevation in aVL with a large amount of ST-depression in lead III.

That alone is diagnostic of a STEMI.

Nothing else will give you that pattern of ST-elevation in aVL with marked ST-depression in lead III. For an example with much more subtle ST-deviations check out this case: The 360 Degree Heart – Part II. Since the “high-lateral” territory is poorly covered by the 12-lead ECG, III and aVL are all is necessary to seal the diagnosis of “high-lateral” STEMI—even without “two contiguous leads” showing ST-elevation.

To make life easier we do have a lead contiguous to aVL showing ST-elevation though: lead I.

Fig. 8. ST-elevation in lead I.

Fig. 8. ST-elevation in lead I.

There’s too much movement to properly assess the precordials on the initial ECG but at this point in our interpretation it doesn’t matter—our patient is experiencing a STEMI. I keep saying it because it’s equal parts simple and important. Once we’ve reached that conclusion, we don’t need to waste time trying to dissect the other leads. Whether the STEMI is lateral, antero-lateral, or antero-septal-postero-lateral (I’m not making up that distribution), our initial management is going to be the same, so time spent searching for further ST-elevation on the ECG is time wasted during the initial phase of our management.

Thankfully, for the curious, we do have a cleaner tracing to work with. It was obtained approximately 20 minutes after the first (and of course there were others performed in-between as well).

Fig. 9. Second ECG.

Fig. 9. Second ECG.

Fig. 10. Precordial ST-elevation on the second ECG.

Fig. 10. Precordial ST-elevation on the second ECG.

On rare occasions you can actually encounter a rate-related STEMI due only to the demand ischemia of an increased heart rate in patients with stable coronary artery disease. For that reason it is important to repeat the ECG after the heart slows down in a case like this to evaluate for resolution of the ischemic changes. In our scenario the ST-deviations are less impressive after slowing but still very evident.

Fig. 11. ECG after rate control.

Fig. 11. ECG after rate control.

So it looks like our patient definitely needs the cath lab…


Bifascicular Block

In addition to his STEMI this patient also has a bifascicular block.

Most of the time bifascicular blocks aren’t that concerning from a prehospital and emergency medicine perspective. Folks walk around with them all the time and until they start experiencing syncope or high-degree AV-blocks the finding is of minimal importance. That stops being true in the patient who is acutely unwell and experiencing a STEMI.

Digressing for a moment, as a specialty we’ve spent years obsessing over “new LBBB” as a criteria for STEMI activation, but it’s actually pretty rare to encounter a truly new LBBB during acute STEMI. Most of what we presume to be “new LBBB’s” are probably chronic findings that just haven’t been documented yet (+/- acute STEMI). That’s because the left bundle branch is a pretty robust system, with the anterior (superior) fascicle supplied by the LAD and the posterior (inferior) fascicle supplied by the posterior descending artery (PDA). Since it receives a dual blood supply, it’s pretty difficult to knock-out both the anterior and posterior fascicles at the same time and create an acutely new LBBB (though it does happen occasionally). Instead, it usually takes long-term processes like aging, fibrosis of the conduction system, or cardiac remodelling to elicit a LBBB.

It’s not often taught or emphasized, but what’s more common (and actually more deadly) during an acute anterior STEMI is a new RBBB. Obviously we still run into the issue of debating whether the RBBB we see is truly “new” or just “new to us,” but because the right bundle branch receives its blood supply solely from the LAD, proximal occlusions of the LAD (or the LMCA supplying it) are more likely to produce a truly new RBBB rather than LBBB.

When that happens it signifies a very high-risk lesion in the proximal coronary arterial tree with a large area of injured and ischemic myocardium. These patients are salvageable but will do poorly without immediate revascularization (and often experience significant morbidity or mortality in spite of our efforts).

So not only does our patient need the cath lab, he needs it as soon as is humanly possible, with the understanding that there is a high likelihood he will deteriorate on the way…


Wide Complex Tachycardia


Fig. 12. Our second ECG in a more rhythm-friendly format.

Fig. 12. This is the ECG from Figure 9 in a more rhythm-friendly format.

The first two tracings demonstrate a fast, mildly irregular, wide-complex tachycardia (WCT). Here’s our differential.

  • Rapid atrial fibrillation or flutter
  • Ventricular tachycardia
  • Sinus tachycardia with frequent PAC’s
  • Atrial fibrillation or flutter with an accessory pathway

Picking the low-hanging fruit, there’s no changing QRS morphology so that makes AF with an accessory pathway highly unlikely. Also, while sinus tach can hide P-waves, the irregularity of sinus tach w/ frequent PAC’s makes it much harder to hide atrial activity during compensatory pauses. I see no convincing atrial activity here so that’s off the table as well. Finally, while the irregularity is somewhat subtle, there’s no pattern to it and again no visible atrial activity, so it’s not a-flutter.

That leaves rapid AF and ventricular tachycardia as possibilities. I know, most folks would have eliminated VT the moment they noted the WCT to be irregular, but I kept it in because it’s both an important diagnosis that affects management and the next-most-likely option after rapid a-fib. I also kept it in because VT can exhibit irregularity in certain situations, including (but not limited to):

  • In the presence of frequent capture and fusion beats.
  • Minor variations soon after onset, while the arrhythmia “settles in.”
  • If there’s a complex scar allowing multiple exit points for the VT.

There is also a slight irregularity to even “regular” VT at times, but it’s usually less than 40 ms of variation and barely perceptible on the surface ECG. What simplifies things for us here is that there are cycle-length variations exceeding 160 ms, ruling out physiologic variation. Also, the QRS morphology is pretty static, ruling-out capture or fusion beats or multiple exit sites.

Really, the only diagnosis we’re left with is rapid atrial fibrillation.


The Shortcut

Of course we don’t have time run through a step-by-step differential like that with a critical patient in front of us, so here’s how I actually diagnosed the rhythm:

  1. I recognized the pattern of massive STEMI with a bifascicular block.
  2. Based on the extensive infarction and “shocked” presentation, I was expecting a compensatory tachycardia like sinus tach or rapid AF.
  3. Knowing the QRS morphology was “typical” for that kind of STEMI, I ignored it as a factor in the rhythm and mostly focused on regularity. It was irregular, ruling-out sinus tach or typical VT and ruling-in AF.

That took all of 10 seconds. Then, when I had a chance a few minutes later, I spent more time dissecting the rhythm to make sure I wasn’t missing anything like irregular VT.



As typically occurs with these cases of STEMI + bifascicular block, there was a lot of confusion over the actual width of the QRS and where to measure the J-point. After spending too much time drawing plumb-lines and playing with a set of screen calipers, I’m calling the true QRS duration 174 ms.

Fig. 13. QRS duration.

Fig. 13. QRS duration.

Turns out I could have saved myself a lot of time because that is the same exact measurement the computer calculated (see Fig. 12). Still, I always say that the sicker the patient is the less you can trust your computerized measurements, so now I can sleep soundly knowing that is probably the right value.



So what happened? The patient obviously got his rate controlled as stabilization (see Fig. 11) and then went for emergent cardiac catheterization where an ostial LAD lesion was identified and removed with suction thrombectomy. Although he now has a residual decreased EF (approx. 35%) and congestive heart failure, he has survived several years since his near-fatal MI and maintains a decent prognosis for the time-being.

For more discussion on the actual management of this case look forward to Part 2 of our conclusion next week.


  • Seth says:

    This was an AWESOME 12 lead. It was a large discussion point for many of my colleagues and I. I look forward to seeing the final conclusion of treatment later on next week. Thanks again for sharing.

  • Matt King says:

    Hey Vince thanks for the through follow up with this case. I am curious how his rate was controlled since he was hypotensive and maybe an unknown onset of when his A-Fib stated(thinking anticoagulation first)? As you know the wrong approach could be devastating in this PT with risks of further infarction, stroke, or death etc… Also why was his rate controlled since it was due to ischemia and not an isolated conduction issue? I could be wrong, but it doesn’t seem the rate(150s) or rhythm was causing his hypotension and may not have even been hurting it too much(obviously not helping) as compared to the ischemic heart and wall motion abnormalities due to infarction/pump failure. To me this case represents a grey area in management with a damned if you do and damned if you don’t approach. Thoughts?

    • I’ll expand on this in the next post but unfortunately I actually wasn’t present for this case so I can’t give my direct account of how things happened. That said, from the notes I read and word-of-mouth from those involved (which I suspect painted things in a better light than I would have viewed them), here’s how he was managed.

      He was initially treated w/ IV normal saline (unknown amount), which brought his BP up to like 108/60-ish. He was then given 20 mg of diltiazem (unknown rate) which brought his rate down from approx. 160 to 130 bpm. An unknown time later his HR increased again to 160-ish and he was sedated with midazolam (unknown dose) and cardioverted x 2. The second cardioversion brought his HR down to 90 bpm (Why? I don’t know), but then he developed hypotension refractory to further IV fluids.

      The cardiologist then “ordered amiodarone and metoprolol” according to the note I saw. Not sure if that means it was given, but that’s what it said. At one point they lost pulses and had to perform a short spell of CPR.
      After the patient regained consciousness he was intubated with etomidate in preperation for transfer.

      I’d say all of that happened in the spell of 90-120 minutes after his presentation to a non-PCI hospital. I’ll get into some more details and my own view of things, but that’s the gist of how his HR was managed. Somehow he did well though, so despite our best efforts to botch things up sometimes the patients just pull through.

  • Billy says:

    Hmmmm, I was fairly close. Sounds like most of the treatment occurred IN Hospital. Love case studies, and that one was good.

  • Dominic says:

    Great discussion on a difficult 12lead! I follow these very closely and based on pt presentation and 12lead tracing, this was a difficult or to treat with impending heart failure, hypotension, and trouble breathing. Thanks for the follow up and look forward to next week!

  • Matt King says:

    Hey Vince thanks for your time, the education, and the follow up. Looking forward to my next piece of FOAM on here.

  • Ken Graurer says:

    Just getting to this one now (after a few hundred comments have already been made … ). VERY NICE presentation and discussion by Vince!

    Although Vince indicated in his detailed analysis that he looks at ST segments first — IF we could place an electronic analyzer within his fine-tuned superbly processing brain — I bet we would find simultaneously-occurring subconscious assessment of the rhythm by Vince — which in this case is irregularly irregular with QRS widening but without clear evidence of sinus P waves. Rather than the “10 seconds” he said this took him — I bet that actually took him less than 2-3 seconds to intuitively process this. At that point — I suspect an innate trained reflex shouted inside of Vince, “Could this be VT?” — which was then refuted by his recognition of LEAD aVL, whose pattern of supraventricular conduction (small q; tall R) with acute MI ST elevation said, “No, NOT VT — but instead a likely large acute MI”. At that point (probably 3 seconds into Vince’s analysis) — I bet Vince noted the “mirror-reflection” reciprocal ST depression in lead III (leads aVL and III are my “go-to leads” when looking for reciprocal change confirmation of acute MI) — at which point Vince said, “Yes, DEFINITE acute STEMI going on!”

    At this point — putting together the pattern now makes sense ( = new-onset rapid AFib + RBBB/LAHB in context of a huge anterior STEMI).

    So — even though on the initial ECG it almost looks like there are P waves in aVL — the gross irregular irregularity without clear P waves in lead II in context with the rest of the ECG says, “I am AFib”.

    And on the original (hard-to-read because of motion artifact) 12-lead — any last vestige of doubt about acute stemi is instantly removed from one look at lead V4, which amidst baseline movement clearly shows ST elevation of acute stemi that is not nearly as easy to recognize in V1,2,3 because of the RBBB.

    GREAT case Vince! –

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