Saturday, April 25, 2020

Another Shark Fin. With a twist.

I was reading stacks of ECGs for a study, without any clinical information.

I came across this one and immediately recognized it and knew the diagnosis (Pendell did too when I sent it to him):
There is a Shark Fin!

What is the diagnosis?

But this is not the kind Shark Fin we usually see, which is due to STEMI! 

This ECG is pathognomonic for severe hyperkalemia.  Wide QRS, large R-wave in aVR, Brugada-like ST Elevation in V1-V3 with inverted T-waves, extremely peaked T-waves (in many leads).

I went to the chart to find the case:

56 y.o. type 1 diabetic presented for evaluation of hyperglycemia. He had stopped taking insulin 5 days prior.  He reported SOB, cough, nausea, and vomiting.

K was 8.4 mEq/L.

pH of 6.96
bicarb 6
pC02 27. 
AG of 32. 

He was immediately given 10 u regular insulin and albuterol for shifting his hyper K. He was started on IVF with pressure bags. 50 mEq of bicarb was given for his severe acidosis. 7u/hr regular insulin drip was started.  

After 30 minutes, repeat labs showed no change in pH or bicarb level. K had improved to 6.9,

Here is the repeat ECG at K 6.9 mEq/L:

And this after K is down to 4.8 mEq/L:

Here are a few other cases of hyperkalemia with PseudoSTEMI:

Here are several cases of Shark Fin due to STEMI

MY Comment by KEN GRAUER, MD (4/25/2020):
GREAT case of “Shark Fin with a Twist”. I’ll suggest a few additional points to those made by Dr. Smith.
  • For clarity — I’ve put the 3 tracings sequentially together in Figure-1:

Figure-1: Sequential compilation of the 3 tracings in this case (See text).

As per Dr. Smith — the initial ECG in the ED ( ECG #1) shows:
  • QRS widening.
  • A large R wave in lead aVR.
  • Brugada phenocopy ST elevation in the anterior leads.
  • T waves that are pathognomonic for hyperkalemia in multiple leads (especially in the inferior and lateral chest leads).
  • PEARL — What I have found most helpful to facilitate instant recognition of hyperkalemia when there is significant QRS widening — is that not only are T waves in many leads tall and peaked — but that these T waves are symmetric (comparable T wave ascent and descent), and these T waves display an extremely narrow base. This will usually be more obvious in some leads than others — but it is unmistakable in leads V4, V5 and V6 of ECG #1.

Additional Features to Note in Figure-1:
  • Marked right axis deviation (predominantly negative QRS in lead I).
  • A relatively long PR interval (if anything, the PR interval is usually shorter with tachycardia).
  • A relatively longer QTc — with a longer-than-expected isoelectric ST segment best appreciated in leads V4 and V5 (which in the setting of hyperkalemia — suggests concomitant hypocalcemia).
  • A pseudo-infarct pattern is also seen in the limb leads (coved ST elevation in lead aVL with reciprocal ST depression in each of the inferior leads).

Sequential Changes — I found it of interest to follow over the course of these 3 sequential ECGs how each of the above additional features resolves as serum K+ normalizes:
  • There is no longer right axis deviation in ECG #3 (the axis is vertical at about +80 degrees, as the QRS is more positive than negative now in lead I).
  • Despite no reduction in heart rate — the PR interval has normalized in ECG #3.
  • The QTc is shorter, without any isoelectric ST segment.
  • The pseudo-infarct pattern in the limb leads has essentially resolved.

Additional Learning Points — The ECG presentation of hyperkalemia is multifaceted. In addition to tall, peaked and pointed T waves + QRS widening + a Brugada-like pattern in anterior leads — there may be:
  • Marked right axis.
  • Associated electrolyte abnormalities.
  • AV conduction defects.
  • Additional pseudo-infarct patterns.
  • Final Point You never know what the underlying ECG will look like until you correct the hyperkalemia and repeat the ECG. This is because whatever ECG findings may have been present before serum K+ increased (ie, ST depression or elevation) — may be masked by the QRS widening and tall, peaked T waves of hyperkalemia. In this case — ECG #3 showed little more than sinus tachycardia and some nonspecific ST-T wave changes.


  1. A good example of acquired Brugada ECG pattern from hyperkalemia. What is Brugada syndrome? A congenitally defective sodium channel resulting in ST elevation in V1-2, subjecting the patient to ventricular arrhythmias. Hyperkalemia and hypothermia can also disable the sodium channel resulting in Brugada ECG pattern. In this case the hyperkalemia is obvious from the T wave morphology, i.e. narrow-based, sharply pointed and tented. So, when one encounters the Brugada ECG pattern in clinical setting, look for hyperkalemis, which is obviously more common than Brugada syndrome.
    K. Wang.

  2. Thank you,at least you took out of my mind this Covid’s time for a while

    1. Thanks for your feedback! Our goal is to keep things going to sustain interest during this pandemic. That said, given seemingly increased inflammatory response + potential thrombotic complications — acute MI remains an important consideration during the Covid-19 era ...

  3. Great post Dr Smith and Ken Grauer, it's very educational. Thanks a lot.As per doctor Amal Mattu said the hyperkalemia is the syphilis of ECGs, because it is The Great Imitator!

    1. Thanks for the kind words! I believe there are 2 "Great Imitators" in ECG interpretation: #1) = Hyperkalemia; and #2) = WPW — :)


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