How to cure incomplete RBBB.

I had an interesting sign-out yesterday. The patient was a 30-ish year old woman with some vague complaint that localized to somewhere between her eyes and her knees. The off-going physician is a model of thoroughness, and they mentioned that the patient was getting, amongst other tests, a CT for pulmonary embolism.

"I wasn't really thinking PE at first," they explained to me, "but after I saw the incomplete RBBB on the ECG, I sent a D-dimer." The D-dimer, of course, came back trivially elevated, and the CT had been ordered.

Ah, the scourge of the IRBBB. It typically take the appearance of an rSR' pattern in V1 and V2 with a narrow QRS, although the AHA takes a dim view of this colloquial definition.

This seemingly "hard" element of evidence, however, can be surprisingly malleable!

I cured the patient's IRBBB!
The patient was already off at CT, so I looked at the ECG myself. It looked pretty darn normal, except for the right-precordial leads:

V2 shows an rSR' pattern, clearly.

The patient returned from CT scan, and I awaited the results. In the meantime, however, I re-interviewed an examined the patient, and convinced myself that she was low risk for all of the "bad actors." The IRBBB stuck in my craw, however, and after some fiddling around, I aquired a new ECG.

Sweet. It's not up there with sinking a difficult tube, or threading a pacer wire, but it makes for a cleaner chart!

What did I do?
I put V1 and V2 where they are supposed to go.

For a fuller explanation of the background here, please check out The most difficult step in obtaining an ECG. It's a post I wrote for paramedics about the importance, as well as the common difficulty, of placing the precordial leads in the correct locations. It's written in a conversational and witty tone, with plenty of illustrations - you'll like it!

Suffice it to say, though, that V1 and V2 are usually placed far too high on the chest. This produces a number of artifacts, including pseudo-infarction patterns and, yes, IRBBB.

I took a picture (with the patient's knowledge and permission - she believes in education!) of the actual lead placements on the patient's chest. The electrode wires are attached to the proper locations, at the 4th intercostal spaces, just to the right and left of the sternum.

Thank you Ms Anonymous!

The other electrode stickers are located only about 5-7 cm higher, around the 2nd or 3rd intercostal spaces, but it was enough to produce the spurious IRBBB.

The Bottom Line
Learn where to put the leads yourself.

If the diagnosis is going to rely critically on the ECG, you ought to check out where the electrodes were placed by the nurse, tech, or paramedic. Certainly, if there are abnormalities isolated to the precordial leads you should go back and do this, especially if the ECG doesn't match the patient's age or presentation.

BONUS QUESTION: For major extra points at the "Port, tell me what electrophysiologic diagnosis may rely on placing V1 and V2 higher than usual.

(Answer can be found by checking my self-aggrandizing link.)

*******
Added post-publication.

Mr Várhegyi points out a similar example, elsewhere on the web, of an IRBBB. Oddly, that example seemed to show some QRS prolongation in V2 that was not appreciated in the other leads.

Source

So, I took another look at my patient's initial ECG:

Darned if it doesn't seem to also have an isolated, minor (< 0.02 seconds), QRS prolongation in V2.

I'm going to defer providing an explanation until I have some idea about why this occurs, or even declaring that this is a reliable feature of improperly placed precordial leads. But it's apparent in these two examples. I'll look into it - anyone else with a better idea write in!

"Mystery" bradycardia, with some irony

Kito and I had an interesting patient last month. 

The patient
I had just been teaching a paramedic student some fine points of the ECG, when nurses asked us to come to room 41.

A 70 y.o. woman was brought in by EMS. She had syncoped when she stood up from the toilet. No zebras there - happens all the time! Her past medical history was about fair for her age; DM2, HTN, CAD, hyperlipidemia, etc, and on Plavix but no warfarin. She had gotten pretty banged up, with injuries to her face and leg.

What really stood out was that her heart rate; around 40. Her blood pressure was stable at 101/66, though, and she denied any chest pressure or trouble breathing.

The ECGs
Her first ECG was obtained at 18:24

A quick check of an old ECG (1 year prior) revealed that the LBBB, at least, was old:

Huh.

The Assessment
A review of her medications from her last ED visit listed carvedilol, and so accidental supratherapeutic dosing seemed likely. Line, labs, and imaging of her injuries were ordered, and we kept a close eye on the monitor.  Her blood pressure stayed north of 100, so we held off on pacers and pressors. Once she was cleared of any traumatic issues, she would be an easy CCU admit. Done.

Ah, not so fast...







 The Denouement

"This is the lab, and we have a critical value to report."

I actually like these phone calls - It's like a Maury Povich-type moment. You know that in the next few moments, all the pieces will fall into place, and you'll either be dancing around in self-congratulation, or applying both palms to your face firmly, rocking back and forth.

It wasn't the troponin, as I had been suspecting.

Instead, it was the potassium that turned up high - a level of 6.6 in fact. For some reason our patient, who had mild CKD before, now had a BUN of 104, and a GFR of 24.

Interestingly, renal and cardiology were not very impressed by the potassium level, feeling that it was a bit low to really cause much trouble. Kito & I had already started treatment, however. After 3 grams of calcium gluconate, the heart rate picked up, and we grabbed another ECG (21:17).

Seemed like we were on the right path, so we started dextrose and insulin, hung normal saline to address the AKI, and eventually gave some Kayexalate (Yes, I know what Weingart said on EmCrit, but a lot of folks still expect you to give it).

The Point

It's not just about tented T-waves.

I'm not going to review all of the protean ways that this electrolyte problem can manifest (please check out the comprehensive article by Matu et al).  I just want to emphasize how it showed up here.

First, there was an unexplained bradycardia, along with PR prolongation. Lastly, there was ST-segment depression in the anterior leads. In retrospect, these were classic signs of hyperkalemia, with plenty of examples from the literature.

Two cases, for example, describes complete AV block, but with a narrow QRS complex. Other cases demonstrate severe bradycardias without tented T-waves or pronounced QRS widening; e.g.

Case 1 from Atropine-resitant bradycardia due to hyperkalemia

You can even see some Wenkebach action, again without the dramatic T- or QRS-wave;

Wenckebach Block due to Hyperkalemia

You get the idea - you can go Google more examples if you want!

And the irony mentioned in the title?
As I mentioned above, I had been teaching ECG stuff to a medic student before this patient came in.  I could have been speaking with her about any number of topics - STEMIs, treating VT, recognizing atrial flutter... But no. 

Of course, it was about recognition of hyperkalemia on the ECG!

STEMI with clean coronaries

The facts: a 35 year old male, with no medical history, presented with 1 week of chest pain that became acutely worse 1 hour prior. It was a "squeezing" feeling that radiated down his left arm. He had some mild dyspnea, and 1 nitro made it somewhat better. Some smoking, no cocaine.

The ECG:

The computer interpretation used CAPS LOCK, and had a lot of "***."

Cardiology was skeptical, but had him in the cath lab 30 minutes later. My resident put 50 cents down on a LAD occlusion, while I bet him a cup of (free) coffee that this was a classic first diagonal , or high lateral, STEMI. The two cardiology fellows agreed that we were both mistaken, and that they were certain to find a blocked circumflex. While the patient was in the lab the troponin came back as significantly elevated.

A few hours later, the cards fellow calls me back with the cath results.

Survey says!

No offense to Steve Harvey, but I'm a Dawson kinda guy.

Nada. Clean cath. "No significant fixed obstructive disease."

Interestingly, however, both ventriculography and an echo revealed hypokinesis of the high anterolateral wall, corresponding to the anatomy suggested by the ECG. He was given a diagnosis of focal myocarditis.

Focal Myocarditis
This isn't very common, but we can't say how uncommon. It is still uncommon enough to be worthy of case reports, at least in Texas. We know that about 3% of MIs (i.e. with positive cardiac enzymes) have clean coronary arteries by angiography, but a number of those people likely have spasm or spontaneous reperfusion. The percentage may even be smaller with true STEMI patterns, but we don't know.

The only way in the past to definitively diagnose myocarditis was through endomyocardial biopsy, which has a good number of shortcomings, both in terms of sensitivity, and of complications.

What could go wrong with this?

Advances in MRI techniques have enabled researchers to noninvasively study myocarditis. In a recent study it was found that 78% of patients who presented with an MI (64% with ST elevation), but a clean cath, had evidence of myocarditis on MRI.

Uh, yeah, I see it too...

Reciprocal changes
Now, I understand that the myocarditis can generate ST elevation, likely in the same manner that pericarditis does. I am really surprised, however, that our patient had such distinctive and appropriate reciprocal changes. Nonetheless, an ECG from a case report of myocarditis also shows reciprocal changes:

Turning to Stephan Smith's ECG Blog for some wisdom, I found this observation in "Is it MI or pericarditis?" (There's a lot of overlap between pericarditis and myocarditis, and many people link them on a spectrum; e.g myopericarditis.):

Pericarditis should never be assumed when there is even a hint of reciprocal ST depression.  Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare.  I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.

A great review article by Punja 2010 gives a few examples of ST elevation in myocarditis, but neither example shows reciprocal changes.

Nasty STE in myocarditis, but no ST depression

Sooo... Rare ECG finding? Not enough research? Incomplete diagnosis?

The Bottom Line

So, the next time you bring in that "for sure" STEMI, keep in mind there's a (3%*78%=) 2% chance it's myocarditis. Or higher. Or lower.