Sunday, August 9, 2015

This ECG is NOT Pathognomonic of Brugada Syndrome

This was contributed by a friend and colleague from a Yale affiliated hospital, Brooks Walsh.

Here is Brooks' case

I had a great opportunity to co-manage a patient with one of my partners, Dr. Charles Mize. He is not only an avid resuscitationist, but also a devoted reader of Dr Smith’s ECG Blog.

A 30-something adult with type 1 DM, but no cardiac disease, presented to the ED with nausea, vomiting, and abdominal pain. They had a history of multiple visits to the ED for gastroparesis (with or without DKA), and their symptoms were stereotypic for prior visits. Analgesia, fluid, and antiemetics were provided, and a basic metabolic panel was sent.

The patient’s symptoms improved, the labs returned, and an ECG was obtained. It was handed to my partner Dr. Mize (since I was at lunch). He activated the cath lab, moved the patient to the resus room, and asked that I finish my soup sooner rather than later.
The computer interpretation read “** ** ACUTE MI / STEMI ** **.”  What does it show?

The ST-segment elevations in V1 and V2 are dramatic, and along with the ST-segment depressions in the inferior and lateral leads could suggest a STEMI. The down-sloping ST-segments with T-wave inversion also could represent a Brugada pattern. However, the QRS is modestly prolonged (about 120 ms in V3), and the ST-segment depressions in the inferior and lateral leads are followed by symmetric, narrow-based, and “peaked” T-waves. This all points to hyperkalemia.

The patient continued to deny chest pain, or that their abdominal pain was different from past episodes. His prior ECG was unremarkable. The potassium was 6.6 mEq/L.

We agreed to provisional activation of the cath lab, although we suspected that we would soon be canceling it. I then performed a point-of-care echocardiogram to assess for gross systolic dysfunction.

A point of care echocardiogram is not an appropriate test to rule-out acute ischemia. However, there was no large wall motion abnormality in the apex (correlating with the ST elevation in V1 and V2). If we had found overt akinesis in that region, we would not have proceeded to our next step.

Dr. Mize administered one gram of calcium chloride IV, and obtained numerous repeat ECGs:

First, right before the CaCl push:
Right before CaCl push

Then during push:
Next, during the CaCl push (note the heart rate increase and jumpy baseline – CaCl burns! Next time I’ll have a running NS line to dilute it):

One minute later:

I texted the ECG and echo clip to the interventionalist, and canceled the activation. Serial troponin levels were undetectable.

Two important lessons from this case

1. Push calcium first!

Our sequence of ECGs demonstrates the rapidity with which calcium can normalize the ECG manifestations of hyperkalemia, reducing the risk of fatal ventricular arrhythmias. There still exists confusion about the optimal approach to treating severe hyperkalemia, with many clinicians still turning to sodium bicarbonate or sodium polystyrene (Kayexalate) as first-line agents, despite the evidence that these agents work very slowly, if at all!

Case reports of hyperkalemia producing “pseudo-STEMI” and/or “pseudo-Brugada” are legion, over decades of the medical literature.  Prior examples can be found on this blog (herehere, and here). 

Two cases on this blog of pseudo-inferior-posterior STEMI due to hyper-K are particularly vexing.  Here is the second one.

But there are also many reports in the formal medical literature:

case report from the NEJM is typical; ECGs were obtained at K=7.9 and K=5.1, with marked improvement in the ECG:

2. Even a K < 7 can produce dramatic ECG changes.
Our patient’s level of only 6.6 demonstrates that even “moderate” levels of potassium can produce severe ECG abnormalities. 

By contrast, the following examples from the literature all had initial potassium levels ranging from 7.0 to over 9!
K = 7.53
Recasens, Lluis, Oona Meroño, and Nuria Ribas. “Hyperkalemia Mimicking a Pattern of Brugada Syndrome.” Revista Española de Cardiología (English Edition) 66, no. 4 (April 2013): 309. doi:10.1016/j.rec.2011.04.021.

K = 9.4
Sims, Daniel B., and Laurence S. Sperling. “ST-Segment Elevation Resulting From Hyperkalemia.” Circulation 111, no. 19 (May 17, 2005): e295–96. doi:10.1161/01.CIR.0000165127.41028.D1.

K = 7.0
Irani, Farzan, Rahil Kasmani, and Yousuf Kanjwal. “Hyperkalemia and Cocaine Induced Dynamic Brugada-Type Electrocardiogram:” European Journal of Emergency Medicine 17, no. 2 (April 2010): 113–15. doi:10.1097/MEJ.0b013e32832e46d1. 

K = 7.0
Littmann, Laszlo, Michael H. Monroe, Lee Taylor III, and William D. Brearley Jr. “The Hyperkalemic Brugada Sign.” Journal of Electrocardiology 40, no. 1 (January 2007): 53–59. doi:10.1016/j.jelectrocard.2006.10.057.

K = 7.7
Kurisu, Satoshi, Ichiro Inoue, and Takuji Kawagoe. “Brugada-like Electrocardiographic Pattern Due to Hyperkalemia.” Clinical Cardiology 32, no. 7 (July 1, 2009): E23–E23. doi:10.1002/clc.20274. 

K = 8.3
Bellazzini, Marc A., and Tom Meyer. “Pseudo-Myocardial Infarction in Diabetic Ketoacidosis with Hyperkalemia.” The Journal of Emergency Medicine 39, no. 4 (October 2010): e139–41. doi:10.1016/j.jemermed.2007.04.024.

Images were reproduced under the "Fair Use" in Copyright Law, which allows such reproduction for non-profit educational purposes.


  1. EXCELLENT POST! That said — I take issue on the semantics of the discussion. The initial ECG IS diagnostic of a Type I Brugada pattern (in my opinion) — since that distinction is based on ECG appearance, which does fit criteria. What differs, is that this is not a spontaneous Brugada pattern, but rather one induced by acute electrolyte/metabolic abnormality (hyperkalemia). Since ECG abnormalities promptly resolve on treatment of the causative factor (hyperkalemia) — clinical implications are NOT as they would be if this ECG picture had been spontaneous. Referral for further evaluation is not necessarily needed ... Again — Excellent post!

  2. Good case, although I'm surprised about the comment re confusion around treatment of hyperkalaemia. The ALS guidelines we have in the UK are very clearly re calcium being first line and it's in all our emergency drug boxes. Never heard of folk using sodium first line. I've got a nice sequence of ECGs I use from a real life case of K 7.0 after 10 then 30mmol CaCl, then after dialysis - shows a nice sequence!

    1. I agree completely, but did not edit that out.
      We always use Calcium first and really bicarb has little effect. Other things that help but take longer are beta agonists, insulin, and furosemide if the patient produces urine.
      Thanks for the comment!
      Steve Smith

    2. "There still exists confusion.." was poor phrasing on my part. The evidence and guidelines aren't confusing, they're quite clear!

      The wide variation in clinical practice, however, can be confusing for medical trainees. They still see some of their mentors pushing IV amps of sodium bicarbonate and PO aliquots of sodium polystyrene. In addition, many EMS protocols in the US continue to list sodium bicarb as first-line for suspected hyperkalemia. This unfortunate situation makes treatment priorities "confusing" for many people, at least in the US.

      Brooks Walsh

    3. Thanks, Brooks - that's very interesting. I don't know quite why but that same confusion doesn't seem to exist over this side of the Pond, the worst I've had is medical students getting fixated on calcium resonium and me having to emphasise that's nothing to do with acute management! (some from certain areas also seem to really like mentioning salbutamol nebs, which have a slight role but nothing compared to calcium chloride!). I think our renal physicians here are pretty strong in their hyperkalaemia teaching when we're students, which helps! Nice case though - thanks :)


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