Saturday, September 5, 2020

A patient with chest pain and ST Elevation in V1 and V2

A 56 year old male complained of chest pain and called 911.

They recorded a prehospital ECG:
As you can see, at the top it says ***Meet ST Elevation MI Criteria***

The medics activated the cath lab prehospital.

It is a pathognomonic ECG.

What is it?

This is hyperkalemia, severe.  Surprisingly, there appear to be P-waves, which are often extinguished when the K is so high.

Severe hyperkalemia often presents with STE in V1 and V2, often with a Brugada-like morphology (tall R in V1, or rSR'; downsloping ST segment; negative T-wave.  There is a very wide QRS and very peaked T-waves.  Especially in V4 and V5, T-waves are peaked because of a narrow base, which is the result of a long flat ST segment (see especially lead III).

Hyperkalemia often results in ST Elevation in V1 and V2 that mimics STEMI.  This is a common pseudoSTEMI pattern! This link has many cases.

On arrival, the hyperK was recognized and the cath lab was cancelled.  The patient was a dialysis patient who missed dialysis the day before.

An arrival ECG was recorded as treatment was started:
QRS duration is 258 ms
It is almost a sine wave.

There are no definite P-waves, but that does not mean that the sinus node is not pacing.  The sinus can still be pacing and conducting, but without any atrial activity to generate a P-wave.  
As Ken states below, this is known as a sinoventricular rhythm

See here examples of sine wave.

Another ECG was recorded 28 minutes later, after treatment with Calcium, glucose and insulin, and 20 mg albuterol nebulization.

The K returned at 9.3 mEq/L
The QRS is now 153 ms.
Notice the ST Elevation with Brugade-like pattern persists in V1 and V2.
Still no definite P-waves.

This was recorded at 60 minutes, after further therapy:
Now the QRS is 137 ms and the STE is gone
There is some undulation of the baseline.  Is this atrial activity?

This was recorded at 2 hours:
QRS is now 101 ms and there only remains a bit of T-wave peaking.
P-waves have returned.

MY Comment by KEN GRAUER, MD (9/5/2020):
As per Dr. Smith — today’s case features a series of pathognomonic ECGs of potential life-saving significance if recognized promptly.
  • Dr. Smith reviews key diagnostic features from the 5 serial tracings that are shown and discussed above. I limit my comments to several additional points regarding the 1st and 3rd ECG that were shown — which for clarity, I have put together in Figure-1.

  Figure-1: The 1st and 3rd tracings shown above in today’s case (See text).

We’ve presented numerous cases of Hyperkalemia on Dr. Smith’s ECG Blog. Today’s case is informative because of the serial nature of findings as they evolve from an initial serum K+ = 9.3 mEq/L — until treatment returns the serum K+ level toward a normal range.
  • I illustrate the “textbook” sequence of ECG findings in hyperkalemia in My Comment at the bottom of the January 26, 2020 post of Dr. Smith’s ECG Blog. Many of these findings are seen in the ECGs from today’s case.

My THOUGHTS on ECG #1: As per Dr. Smith — the initial prehospital tracing on the 56-year old man in today’s case ( = ECG #1) — is pathognomonic for hyperkalemia.
  • The QRS complex is markedly widened.
  • There is marked bradycardia (rate in the 40s).
  • P waves appear to be present in some places (RED arrows in lead V1) — but P wave amplitude is markedly reduced.
  • Conduction defects are present. Judging from the P waves we see for the 2 QRS complexes in lead V1 (RED arrows) — the PR interval appears to be constant, and markedly prolonged (1st-degree AV block).
  • The presence of P waves elsewhere is less certain. That is — I’m less certain that the question marks in leads I and II represent atrial activity. With progressive hyperkalemia — P wave amplitude decreases until ultimately P waves disappear. Interestingly, the sinus node is often still able to transmit the electrical impulse to the ventricles, even though no P wave may be seen on ECG. This is known as a sinoventricular rhythm — which if not intermittently present in ECG #1  is seen later on in this case.
  • T wave morphology in ECG #1 is telling. As I illustrate in the January 26, 2020 post — these T waves resemble the Eiffel Tower (ie, not only are T waves in multiple leads of ECG #1 tall, peaked and pointed — but these T waves are symmetric with an equal angle of rise and fall — with a very narrow T wave base)KEY Point: These T waves in leads II, III, aVF; and V3-thru-V6 of ECG #1 are too thintoo symmetric, and have too narrow of a base to be either a repolarization variant of deWinter T waves.
  • Finally — a Brugada-1 ECG pattern is seen in leads V1 and V2 of ECG #1. This is almost certainly a Brugada Phenocopy. As per Dr. Smith — it is common to see Brugada Phenocopy in association with severe hyperkalemia.

Regarding BRUGADA Syndrome vs Phenocopy: We’ve presented many cases of Brugada ECG patterns on Dr. Smith’s ECG Blog. For an excellent State-of-the-Art Review on Brugada Syndrome — Please SEE this article by Brugada et al in JACC — Vol. 72; Issue 9; 2018.
  • A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-2).
  • A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or V2 positioned normally — or positioned 1 or 2 interspaces higher than usual) — or — a Brugada-1 pattern may be observed on provocative drug testing after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
  • NOTE #1: In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. This definition was changed following an expert consensus panel in 2013 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern, without need for additional criteria.
  • Panel B in Figure-2 illustrates the Brugada Type-2 or “Saddle-back” ECG pattern. This pattern may be suggestive — but is not diagnostic of Brugada Syndrome (See Figure-2).
  • NOTE #2: A number of conditions other than Brugada Syndrome may temporarily produce a Brugada-1 ECG pattern. These include (among others) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia/infarction/cardiac arrest — and hyperkalemia. Patients with such conditions that may transiently mimic the ECG findings of a Brugada-1 pattern are said to have Brugada Phenocopy. The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, hyperkalemia in today’s case) may result in resolution of the Brugada-1 ECG pattern, with a much better prognosis compared to patients with true Brugada Syndrome. Note in the last (5th) ECG shown above in today’s case — that there is no longer any hint of a Brugada-1 or Brugada-2 pattern.

Figure-2: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol. 72; Issue 9; 2018) — (A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. (B) Brugada-2 ECG pattern (the “Saddle-back” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave. (C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOPthe ß-angleBOTTOMA Brugada-2 pattern is present if 5 mm down from the maximum r’ rise point — the base of the triangle formed is ≥4).

Returning to Figure-1: I’ll complete my comments with a look at ECG #3 — which was obtained 28 minutes after today’s patient arrived in the ED (following treatment with calcium; glucose + insulin; and albuterol nebulization).
  • Although still wide — the QRS complex in ECG #3 is not as wide as it was in ECG #1.
  • The rate is a little faster (ie, ~60/minute) — but I no longer see any sign of P waves. Presumably — this is now a sinoventricular rhythm.
  • T waves are still tall, peaked and pointed — although not quite as tall as they were in ECG #1.
  • NOTE #3: We are beginning to see ST depression in ECG #3 — especially in the inferior and lateral precordial leads. This is clearly more marked than it was in ECG #1. It’s important to appreciate that the ECG effect of severe hyperkalemia may mask other underlying ST-T wave abnormalities. Only on repeat ECG, after serum K+ returns to normal will we be able to accurately assess for the presence or absence of acute ST-T wave changes.
  • NOTE #4: I found it interesting that certain leads in ECG #3 (especially leads aVL, V2) — look much narrower than they really are. This highlights the importance of using all 12 leads to assess for QRS duration. I’ve added 2 sets of vertical lines in ECG #3 — in which the vertical BLUE line marks the onset of the QRS complex (as seen in the long lead II rhythm strip) — and the vertical PURPLE line marks the end of the QRS. The reason the QRS complex in certain leads looks deceptively narrow — is that part of the QRS in those leads lies on the baseline.
  • NOTE #5: As per Dr. Smith — a Brugada-1 ECG pattern persists in leads V1 and V2 in ECG #3. In addition — we now also see a Brugada-2 (saddleback) ECG pattern in lead V3! That said — the fact that the last (5th) ECG done in this case shows no trace of any Brugada-type pattern essentially confirms we were seeing Brugada Phenocopy associated with severe hyperkalemia on the earlier tracings.


  1. Steve and Ken...

    An excellent presentation with a primo discussion and great ECG examples.

    I just have two comments to add to this: Generally, the only time a true Brugada Syndrome patient has symptoms (related to the Brugada Syndrome) will be during a ventricular tachycardia or V-fib. So, their ECG won't look like a straight-forward Brugada Syndrome at that point. The age range that one usually sees in this syndrome is a bit young to be suffering from ischemic heart disease. A 56 y/o male is a bit old to be diagnosed with Brugada Syndrome for the first time.

    So the bottom line is: if you fortuitously discover what you believe to be a Brugada Syndrome in a patient, unless they are presenting post-resuscitation or immediately post-syncope... their risk usually involves a long-term prognosis. But if you see what you think is a Brugada Syndrome in a patient who appears distressed and does not fit the typical picture for a Brugada Syndrome patient (young male, post-syncope, +FH), think first in terms of hyperkalemia because their "risk" is already occurring.

    The second comment is that hypercalcemia can do this, too, but it usually doesn't look as much like a Brugada Phenocopy as hyperkalemia.

    Jerry W. Jones, MD FACEP FAAEM

  2. super cool case. at first glance i, like the medics, thought "STEMI". but then i thought: why is Dr Smith showing this.. it's not what it seems at first glance (and i never look at the computer read)... then thought "wide ugly QRS, T's look like they'd hurt if i sat on one, brady, hidden P's and said yep: hyperK.
    the Brugada phenotype discussion was cool.
    am reading Parrillo's Crit Care text for RLA, just finished the AKI chapter. interestingly, the treatments we give to pull the patient back fro the cliff of sine-waves and death, ie, calcium, d50/insulin, nebs, ? sodium bicarb, are all transient, lasting about 2 hours i think.
    which means i need to be sure the patient is dialyzed stat.
    thanks guys.

    1. THANKS so much Tom! Yes — this patient needed stat dialysis! — :)


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