Friday, July 23, 2021

ECG Blog #244 (58) — The Cath Lab Was Activated. Do You Agree?


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ECG Blog #244 (MP-58) — The Cath Lab Was Activated. Agree?



The ECG in Figure-1 was obtained from a non-English speaking adult male, who presented with acute abdominal pain. The patient had a known history of diabetes — but because of the language barrier, the history was otherwise extremely limited.

  • On seeing the ECG in Figure-1 — the cath lab was activated.



  • Should the cath lab have been activated?
  • Explain your answer.



Figure-1: ECG obtained from a non-English speaking adult man with a history of diabetes and acute abdominal pain. The cath lab was activated. Do you agree?



NOTE: Some readers may prefer at this point to listen to the 8:30-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-58).


Today's ECG Media PEARL #58 (8:30 minutes Audio) — Reviews some lesser-known Pearls for ECG recognition of Hyperkalemia.



MY Sequential Thoughts on the ECG in Figure-1:

As much as I "preach" the need to be systematic in ECG interpretation (as reviewed in detail in ECG Blog #205) — my "eye" was instantly drawn to several KEY findings for the ECG shown in Figure-1. This immediately suggested 2 ECG diagnoses to me.



  • What are the 2 ECG diagnoses that should come to mind within seconds of seeing the ECG in Figure-1?






  • A Brugada-1 ECG pattern is seen.
  • Significant hyperkalemia is probably present.



PEARL #1: As important as a systematic approach to ECG interpretation is — the experienced clinician will with some ECGs immediately (almost automaticallyknow within seconds what is going on. When you encounter this — LISTEN to what the ECG is telling you. Sometimes this instinctive (almost automatic) diagnosis that you instantly "just know" may require immediate treatment (as when you see a wide tachycardia and know from the ECG appearance that the rhythm is VT). Therefore — Allow yourself a quick 5-10 seconds to "take in" any diagnosis that just "comes" to youThen go back to the ECG — and complete your systematic interpretation.

  • In Figure-1 — the importance of rapidly recognizing the Brugada-1 ECG pattern with probable severe Hyperkalemia is that: i) Immediate treatment of the hyperkalemia is needed; and, ii) Both of these conditions may dramatically alter ECG appearance in a way that will hinder systematic assessment if you don't realize these conditions are present. This happened in today's case — as initial providers mininterpreted the ECG in Figure-1 as suggestive of an acute STEMI, and therefore activated the cath lab.



The Brugada-1 ECG Pattern:

As illustrated and discussed in detail in ECG Blog #238 — the shape of the extreme (almost 10 mm) coved ST elevation in leads V1V2 and V3, that terminates in T wave inversion is diagnostic of a Brugada-1 ECG pattern. This is especially true for the picture we see for the QRST complex in lead V1.

  • This image of the QRST complex in lead V1 should be "engrained" in our brains — as a visual sign that immediately says, "I'm a Brugada-1 ECG pattern".
  • While understandable that the overwhelming amount of ST elevation in anterior leads V1, V2 and V3 might prompt concern for a large anterior STEMI — the 2nd ECG diagnosis that our "experienced eye" has already made ( = hyperkalemia) — makes it much less likely that there would also be an ongoing STEMI.
  • P.S. One might also misinterpret the rSR' in lead V1, with wide terminal S waves in leads I and V6 as consistent with RBBB. While true that this QRS morphology is consistent with RBBB — simple RBBB does not produce the ST segment shape that we see in each of the first 3 anterior leads, in which the dramatically elevated ST segments are coved (in V1,V2) and voluminous, taking a very delayed path in their descent toward final T wave inversion. NOTE: While I can not rule out the possibility that there is also underlying RBBB from this single tracing — what we know is that there is a Brugada-1 ECG pattern!


PEARL #2: As emphasized in ECG Blog #238 — a number of conditions other than Brugada Syndrome may temporarily produce a Brugada-1 ECG pattern. Among these other conditions — Hyperkalemia is perhaps the most common.

  • Development of a Brugada-1 or Brugada-2 ECG pattern as a result of some other condition — with resolution of this Brugada ECG pattern after correction of the precipitating factor(s) is known as Brugada Phenocopy. The importance of recognizing Brugada Phenocopy — is that the risk of malignant arrhythmias is far less than it is for Brugada Syndrome.
  • Regardless of whether one was still concerned that the ST elevation in Figure-1 might also represent an ongoing STEMI — Severe hyperkalemia would need to be treated before acute cath (and before any potential intervention for acute MI) could be contemplated. Therefore — the initial management approach to this patient is essentially defined within the few seconds it should take to recognize the severe hyperkalemia and Brugada-1 pattern on ECG (ie, promptly beginning with IV Calcium, even before lab confirmation returns).
  • Whether the ECG changes in Figure-1 represent Brugada Phenocopy or Brugada Syndrome — and/or a STEMI — is almost certain to become apparent with ongoing monitoring of the serum K+ level — treatment of any other predisposing conditions — and through serial ECGs, that should show marked improvement, with resolution of ST elevation as serum K+ is corrected IF the ECG changes in Figure-1 are the result of Brugada Phenocopy.



The 2nd ECG Diagnosis = Severe HyperKalemia:

For clarity — I've added Figure-2, which presents the "textbook" sequence of ECG findings seen with progressive degrees of hyperkalemia. While fully acknowledging that "not all patients read the textbook" — and that there will be variations in the various ECG findings from one patient-to-the-next — I have found awareness of the generalizations for these ECG signs in Figure-2 to be extremely helpful.

  • The usual earliest sign of hyperkalemia ( = T wave peaking) may begin with no more than minimal K+ elevation (ie, K+ between 5.5-6.0 mEq/L) — although in some patients, T wave peaking won't be seen until much later.
  • I love the image of the Eiffel Tower. With progressive degrees of hyperkalemia — the T wave becomes tall, peaked (pointed) with a narrow base. While patients with repolarization variants or acute ischemia (including the deWinter T wave pattern) often manifest peaked T waves — the T waves with ischemia or repolarization variants tend not to be as pointed as is seen with hyperkalemia — and, the base of those T waves tends not to be as narrow as occurs with hyperkalemia.
  • P.S. As helpful as I find Figure-2 is for providing insight to the ECG changes we look for when suspecting clinically significant hyperkalemia — progression from sinus rhythm to VFib as the 1st ECG sign of hyperkalemia has been documented. Not all patients read the textbook. (emDocs, 2017 — Management of Hyperkalemia).



Figure-2: The "textbook" sequence of ECG findings with hyperkalemia.



ECG Changes of Hyperkalemia in Today's Case:

The reasons I instantly suspected severe hyperkalemia in today's case were:

  • Significant QRS widening (to at least 0.11 second in leads I, II, aVL and others).
  • T wave morphology that is typical for hyperkalemia. As shown in Figure-3 — the T waves in multiple leads resemble the Eiffel Tower (ie, not only are the T waves in leads I, II, aVL; V4, V5 and V6 tall, peaked and pointed — but these T waves are symmetric with an equally steep angle of rise and fall — with a narrow T wave base).
  • There is a Brugada-1 ECG pattern in leads V1, V2 and V3. As emphasized above — it is common to see Brugada Phenocopy in association with severe hyperkalemia.


Beyond-the-Core: Did YOU notice the "hump" in lead V3 (BLUE arrow). I believe what we are seeing in this lead is the pointed peak of what the T wave in lead V3 would have looked like — were it not obscured by the Brugada-1 pattern.

Figure-3: Take another look at the ECG in today's case. Don't YOU See the Eiffel Tower effect for the T waves in multiple leads?



PEARL #3: Assessment of the rhythm with severe hyperkalemia is often extremely difficult because: i) As serum K+ goes up — P wave amplitude decreases, and eventually P waves disappear (See Panels D and E in Figure-2)ii) As serum K+ goes up — the QRS widensandiii) In addition to bradycardia — any form of AV block may develop, and AV conduction disturbances with severe hyperkalemia often do not "obey the rules" (See Figure-4).

  • THINK for a MOMENT what the ECG will look like IF you can't clearly see P waves (or can't see P waves at all) — and the QRS is wide? ANSWER: The ECG will look like there is a ventricular escape rhythmor like the rhythm is VT if the heart rate is faster.
  • NOTE: We do not see P waves in most of the leads in Figure-3 — and it's difficult to be certain if the deflection in lead II is a sinus P wave (RED arrow). Fortunately — a definite P wave is seen in lead aVF, which confirms that the rhythm is still sinus (ie, sinus tachycardia at ~135/minute). But without lead aVF — I would not have been at all certain what the rhythm was.


Figure-4: Why assessing the rhythm with hyperkalemia is difficult (See text).



Follow-Up to the Case:

The cardiac cath was negative (Clean coronary arteries! ). That said — the patient's condition precipitously declined after catheterization — and he was emergently intubated. Pertinent lab findings on admission included a pH = 6.94 — glucose over 1,100 mg/dL — serum K+ = 7.5 mEq/L.

  • Fortunately — the patient's DKA (Diabetic KetoAcidosis) responded to treatment, with normalization of lab values.
  • I was unable to obtain follow-up ECGs that could have confirmed my suspicion of Brugada Phenocopy.



Acknowledgment: My appreciation to David Didlake (from Texas, USA) for allowing me to use this case and these tracings.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
  • ECG Blog #238 — Reviews Brugada Syndrome vs Brugada Phenocopy. 

  • The January 26, 2020 post in Dr. Smith's ECG Blog — Reviews a number of examples of hyperkalemia (with My Comment at the bottom of the page). 
  • The September 5, 2020 post in Dr. Smith's ECG Blog — Reviews another case of Brugada Phenocopy from Hyperkalemia (with My Comment at the bottom of the page). 
  • The April 25, 2020 post in Dr. Smith's ECG Blog — One more case Brugada Phenocopy from Hyperkalemia + "Shark Fin"-like ST Elevation (with My Comment at the bottom of the page). 
  • The October 21, 2020 post in Dr. Smith's ECG Blog — Reviews a case of Hyperkalemia which highlights the difficulty of determining the Rhythm (with My Comment at the bottom of the page).


  1. how to differentiate hyperK from Na blocker toxicity in ECG since they both affect Na channel.
    Example 2 from ""Tricyclic Overdose • LITFL • ECG Library "" look both fit criteria for hyperK adm TCA intoxication

  2. LITFL list the following as “ECG features of Sodium-Channel Blockade” — sinus tachycardia — QRS widening — right axis deviation — R/S ratio >0.7 in aVR. You are correct that some of these indicators DO resemble what can be seen with hyperkalemia. HISTORY may be very helpful (ie an overdose vs acute renal failure) — plus with hyperkalemia, there tends to be more of the characteristic “Eiffel-Tower-like” T wave changes (ie, very tall AND skinny and pointed T waves) — though as shown on LITFL in their Examble 1b — the ECG picture of these 2 conditions may sometimes look quite similar (Look for Example 1b here — )

  3. With a HX of DM, immediately HyperK came to mind. Nice EKG.

    Hurry back and take care.

    1. Exactly! "Common things are common" — and it REALLY helps (as you indicate) to begin narrowing the differential based on ALL the information that we have — :)