As is usually the case with tracings contributed by Sebastian Garay — “C’est bizarre” (ie, This one is a doozy! ). All we are told is that the patient is a 28-year old woman who was found at home, unresponsive. This opens up a host of potential diagnoses.

The Rhythm — is unusual! As Dawn astutely detected — the rhythm is almost-but-not-quite regular. Using CALIPERS is essential for proceeding further — since there is not much difference in R-R intervals on this tracing. But IF you use calipers — you can verify my observation that there is a pattern to this rhythm! That is, every 3rd R-R interval is slightly longer! (ie, color-coded shorter BLUE vs slightly longer RED double arrows in my attached Figure). This regular-irregularity pattern of “group beating” essentially rules out sinus tachycardia — and makes me highly suspicious of Wenckebach exit block out of the AV node.

Proceeding further with description of the rhythm — I do not see clearly defined P waves, although (as per Dawn) — there may indeed be atrial activity in lead V2 (See regularly-occurring slanted RED lines at ~300/minute in lead V2). Although the QRS complex is wide — QRS morphology clearly resembles the supraventricular etiology of RBBB (qR in V1 + wide terminal S waves [within RED circles] in leads I and V6). Although AFlutter almost always manifests at least some sign of regular atrial activity in more than a single lead — I am at a loss to explain this rhythm any other way! AFlutter is the only rhythm producing regular atrial activity at an atrial rate close to 300/minute (which we seem to see in lead V2, albeit not in other leads) — and, it is common for AFlutter to manifest unusual patterns of group beating due to various conduction ratios resulting from multi-level Wenckebach block out of the AV node.

I suspect that in addition to the RBBB described above — that there is also a Brugada-1 pattern in lead V1 (within the BLUE rectangle). This is almost certainly a Brugada Phenocopy — which means that rather than a true Brugada “Syndrome” — we transiently see a Brugada-1 ECG pattern as the result of some other underlying cause — and that when this precipitating cause is corrected, the ECG will normalize. This is important clinically for risk assessment — since morbidity and mortality from Brugada-pattern ECGs is significantly less in patients with Phenocopy rather than the true “Syndrome”. (CLICK HERE to take you to 9:17 in in my 29-minute ECG video on Brugada ECG Patterns. IF you click on SHOW MORE under the video in the YouTube page — You’ll find a full linked Contents to all in this video).

In addition to RBBB — there is also marked RAD (Right Axis Deviation). Given rS morphology in lead I — and qR morphology in each of the inferior leads — this is consistent with a bifascicular block pattern of RBBB/LPHB (Left Posterior HemiBlock).

Finally — Moving to assessment of the ST-T waves — this is complicated because IF the rhythm is in fact AFlutter — atrial flutter activity may alter the appearance of the ST-T wave in any lead. That said — the predominant finding in virtually ALL leads on this tracing is tall, peaked and pointed T waves with a narrow base. To me, this appearance suggests significant hyperkalemia until you prove otherwise!

Of NOTE — hyperkalemia can produce numerous unusual ECG findings, that then “go away” once the hyperkalemia is corrected. Hyperkalemia is a common cause of Brugada Phenocopy — so repeating this ECG after hyperkalemia is corrected might result in complete resolution of the Brugada-1 pattern we see in lead V1. Hyperkalemia might also produce marked axis deviation (as we see from the predominantly negative QRS in lead I).

BOTTOM LINE: As per Dawn — clinical correlation is essential to this case. Given that this is a younger adult who was found unresponsive — we need to add Sodium Channel Blocker Overdose (given tachycardia, QRS widening with right axis, terminal R’ in aVR and Brugada-1 pattern in lead V1). We also need to add other causes of unresponsiveness that might produce marked hyperkalemia (with acute DKA being high on that list).

Follow-Up: As noted by Dawn — Sebastian confirmed DKA with serum K+ = 8.2 mEq/L at the time this tracing was obtained. I’d LOVE to see a follow-up ECG after DKA resolves, after serum K+ corrects, and when the patient has woken up.

Our THANKS again to Sebastian Garay for another SUPER contribution!

Dawn...

What a GREAT ECG and my thanks to Sebastian Garay for the opportunity to see this. Also, great discussions by YOU and Dr. Grauer.

First and most importantly, we are diagnosing this dysrhthmia (as well as the rest of the ECG) from a 12-lead ECG. Never - let me repeat that - NEVER - diagnose a dysrhythmia from a rhythm strip. The width of the QRS depends on the orientation of its vector in each lead. It is quite possible (I have examples that I use to trip up my students in my advanced ECG classes) that a wide QRS rhythm may have a vector orientation causing the terminal portion of the QRS in one or more leads to be essentially isoelectric. This will cause that lead to appear to have a normal, narrow QRS complex.

After reviewing the rhythm, intervals etc...

One of the first things that caught my eye was the QRS-T complexes in V1. It looks very much like a Brugada syndrome, but I was also immediately impressed that it wasn't. First, the patient is a 28 y/o female. That alone would be very, very unusual for a Brugada syndrome (not impossible, though). Second, the tall, narrow and sharply peaked T waves are so very characteristic of hyperkalemia. And, all cases of hyperkalemia with ST elevation that I have seen - except for ONE! - has looked very similar to the Brugada Type 1 changes in V1. One case was indeed essentially indistinguishable from an acute epicardial ischemia. So at this point I'm thinking hyperK+.

At this level of the serum K+, the patient's heart is likely experiencing a sinoventricular conduction; therefore, no obvious P waves.

Now to the altered consciousness. A systolic BP of 99 should not render anyone unconscious unless 1) it had just recovered from being 30/0, 2) her systolic BP is usually around 180, 3) there is a medication or drug on board or 4) there is a metabolic issue. I would hazard a guess that it wasn't either of the first two (but that would just be a clinical hunch) and would look at reasons 3 or 4. I've seen a number of Class I antidysrhythmic OD's during my time and they all presented with really wide QRS complexes (even some of the Class Ib when taken in overdose). That includes tricyclic antidepressants, also. Based on this ECG, I would put those drugs on the back-burner but that still doesn't R/O other recreational drugs. Check the pupils. If I weren't immediately impressed with any findings suggestive of drug overdose, then I would consider some sort of metabolic derangement. Of course, I'm already leaning heavily toward hyperK+, but other similar cases I've seen in the emergency department over a 40 yr career include hypercalcemia, diabetic ketoacidosis (of course), myxedema coma, central pontine myelinosis and acute adrenal insufficiency. I think a quick sniff of her breath would tell us the result here. Often in these patients, you can smell the ketones as you begin to approach them.

But based strictly on the ECG, I would first consider the sharply peaked T waves (nothing else creates narrow-based T waves that come to THAT sharp of a peak) which for me makes Brugada syndrome much less likely, the repolarization changes in V1 which also look exactly like the STE of hyperkalemia as well as Brugada syndrome but I strongly favor hyperK+ here, and the narrow QRS which is validated in all the leads and not just in one rhythm strip which makes Class I antiarrhythmic and tricyclic overdose much less likely. For me, the metabolic disorder (other than hyperK+) is not obvious on this ECG. I would have had to see the patient in person or else know her serum glucose and acid/base status as well as other electrolytes to verify that.

Quite honestly, I've seen hundreds of DKA's during my career (probably hundreds before I finished residency) but I do not recall having seen one with a K+ level THAT high.

That being said, please allow me to soap box a bit here. Nothing - absolutely nothing - in medicine and especially in electrocardiography is 100%. Recently, on various blogsites, I have seen some contributors criticized for making a statement because someone points out that THERE IS AN EXCEPTION TO THAT STATEMENT! OF COURSE there are exceptions! There is ALWAYS - and I mean ALWAYS! - an exception somewhere. This does not bother me in the least when I make a decision based on a reasonable probability that something has occurred. Obviously, if you have to choose between two diagnoses and one occurs 49% of the time and the other 51% of the time, you'd better NOT use probability of occurrence in your decision. But when you are choosing between 2% and 98%, I find NO PROBLEM using that data to make a decision. I do it ALL THE TIME! Otherwise, you'll find yourself like a first year resident that suddenly faces his or her first life or death decision paralyzed by fear and indecision.

Thanks for maintaining a GREAT website and for allowing others to voice their opinions and perhaps provide a little knowledge for all of us.