What is this ST Elevation?

This patient was sent to the ED because of a potassium of 6.1 mEq/L and some acute renal insufficiency.

He had an ECG recorded:

This was brought to me for analysis.  

The computer read "Septal Myocardial Infarction"

What do you think?

There is saddleback ST Elevation and Q-waves in leads V1 and V2.  

Whenever I see a saddleback, or Q-waves in V1, V2, I look to see if the leads were placed too high.  

How would I know?  By looking at the P-wave in lead V2, which should always be upright. Furthermore, the P-wave in lead V1 should almost always be biphasic up-down.  In this ECG, the P-wave is fully inverted in both leads.  This is common and due to leads V1 and V2 placed too high.  

Leads V1 and V2 should be in the 4th intercostal space.  Leads V4-V6 should be in the 5th.  

Furthermore, Saddleback STE in V2 is rarely due to acute LAD OMI.   

I have seen only 2 such cases ever.  One was incredibly subtle.  

They are both here: http://hqmeded-ecg.blogspot.com/search/label/Saddleback%20STEMI

I said there is nothing to worry about here.  But to record another one with the leads placed correctly.  

Here it is:

P-waves are biphasic in V1 and upright in V2. The Saddleback is gone. The ST elevation is typical for the depth of the S-wave. There is likely LVH.  

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MY Comment by KEN GRAUER, MD (4/17/2022):

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I found today's case interesting because of the interplay between: i) Potential ECG effects of Hyperkalemia (ie, the patient was sent to the ED for evaluation because of an elevated serum K+ = 6.1 mEq/L); ii) A Pseudo-Infarct Pattern with large antero-septal Q waves and a "saddleback" form of ST elevation that resembles a Brugada-2 pattern; iii) Misplacement of the lead V1 and V2 electrodes; and, iv) LVH (Left Ventricular Hypertrophy).

I focus my comments on addressing these 4 interacting factors. As per Dr. Smith — there is no indication for concern about acute coronary occlusion from the initial ECG in today's case.

• For clarity — I've put together and have labeled the 2 ECGs in today's case (Figure-1).

Figure-1: The 2 ECGs in today's case.

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3 Clues to Quickly Recognize V1, V2 Misplacement:

As emphasized by Dr. Smith — one look at ECG #1 should immediately suggest too-high placement of the lead V1 and V2 electrodes on the chest. As per My Comment at the bottom of the page in the November 4, 2018 post in Dr. Smith's Blog — I favor use of 3 Clues. To summarize — Suspect leads V1 and/or V2 have been placed 1 or 2 interspaces too high on the chest IF one or more of the following clues are present:

• CLUE #1 — If there is an r’ in leads V1 and/or V2, especially if the other finding for incomplete RBBB (ie, terminal s waves in lateral leads I and V6) is absent.
• CLUE #2 — If there is a significant negative component to the P wave in lead V1 and/or V2.
• CLUE #3 — If the appearance of the QRS complex and the ST-T wave in leads V1 and V2 looks very much like the QRS and ST-T wave in lead aVR.

All 3 of these clues are at least partially suggested in ECG #1 (within the RED rectangles for the TOP tracing in Figure-1).

• A terminal r' (terminal positive deflection) is seen in both leads V1 and V2. 
• Both leads V1 and V2 manifest a significant negative component to their P waves (RED arrows in these leads).
• Although the ST segment flattening seen in lead aVR is different from the ST-T wave appearance in leads V1 and V2 — the distinctive QRS morphology (a Qr' pattern) is virtually identical in all 3 leads within the RED rectangles.

Potenial Caveats regarding the 3 Clues:

As helpful as the above 3 Clues are for quickly suspecting too high placement of leads V1 and/or V2 — these clues are not infallible. There are times when despite our suspicion from looking at an ECG that leads V1 and V2 have been placed too high — this will turn out not to be the case. Consider the following:

• There may normally be a negative component to the P wave in leads V1 and/or V2 — especially if atrial size and/or pressure is increased (ie, one of the ECG criteria for left atrial abnormality is a deep negative component to the P wave in lead V1). That said, most of the time — the depth and width of a “normal” negative component to the P wave in leads V1 and/or V2 will not be nearly as prominent, as it is in leads V1 and V2 of ECG #1.
• Physiologically — the presence of a terminal r' deflection means that the last component of ventricular depolarization (from the viewpoint of leads V1 and V2) is directed toward the right (ie, toward the right ventricular outflow track). An r’ in lead V1 (and even incomplete RBBB) are not necessarily abnormal findings in a small but significant percentage of otherwise young, healthy adults — since ventricular depolarization of this portion of the RV is sometimes slightly delayed relative to LV depolarization as a normal phenomenon. That said, it is far less common to see a terminal r’ in lead V2 of an otherwise healthy adult — although it still is possible.
• Variation in body habitus and chest wall anatomy may also sometimes account for unexpected ECG findings — and in today's case, hyperkalemia is an additional potential confounding factor.
• BOTTOM LINE — As per Dr. Smith, it is EASY to follow-up on your suspicion that leads V1 and/or V2 may have been placed too high on the chest: Simply verify lead placement yourself, as YOU repeat the ECG! As is evident in ECG #2 in Figure-1 — the repeat ECG shows: i) Loss of the negative component to the P wave in leads V1 and V2 (BLUE arrows in these leads); ii) Loss of the terminal r’ in leads V1 and V2; iii) Loss of the Q wave in lead V2; and, iv) loss of any resemblance between the ECG appearance of leads V1 and V2 with lead aVR. This confirms leads V1 and V2 were placed too high on the chest in ECG #1!

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The "Saddleback" in Figure-1 is Not a Brugada-2 Pattern:

No matter how many times I see Brugada-1 and Brugada-2 ECG patterns — I still find myself referring to the images in Figure-2, that I have reproduced from My Comment at the bottom of the page of the September 5, 2020 post in Dr. Smith's Blog.

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 (TOP: the ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum r’ rise point — the base of the triangle formed is ≥4).

Regarding today's case — when I first saw the ST-T wave appearance in leads V1 and V2 in ECG #1 — I considered that this might represent a Brugada-2 ECG pattern. While this "saddleback" morphology of upward-sloping ST elevation is not by itself diagnostic of Brugada Syndrome — it would raise this possibility.

• The above said — a Brugada-2 ECG pattern is not present in leads V1 and V2 of ECG #1. Note in Panel C of Figure-2 illustration of a widened ß-angle as a key component for the diagnosis of a Brugada-2 pattern. Contrast this to the extremely narrow ß-angle for the r' deflections in both V1 and V2 in Figure-1.
• As noted earlier — a terminal r' deflection in lead V1 is an extremely common normal variant finding in otherwise healthy young adults. In today's case — not only did the terminal r' deflections in leads V1 and V2 of ECG #1 not represent a Brugada-2 pattern — but these terminal r' deflections disappeared once the ECG was repeated with correct lead placement!

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Anterior T Wave Peaking (Hyperkalemia and/or LVH)?

We are left with explaining the anterior lead T wave peaking seen in both ECGs in Figure-1. I completely agree with Dr. Smith that there is nothing to suggest acute coronary occusion in today's ECGs. But I feel it important to: i) Be aware of all the potentially interacting factors in today's case; and, ii) To appreciate that we will not know what the "true" ST-T waves look like in today's patient until serum K+ is corrected from the elevated 6.1 mEq/L value recorded on arrival in the ED.

• The "good news" — is that the repeat ECG after correcting lead placement eliminated the large Q wave that had been seen in lead V2 of ECG #1. But tall, peaked T waves persisted in the anterior leads of ECG #2.
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• LVH is an interacting factor. I've reviewed on a number of occasions the approach I favor for ECG diagnosis of LVH (See My Comment in the June 20, 2020 post of Dr. Smith's Blog, among others — and See Figure-3 for specific criteria I use). Even not knowing the age and sex of today's patient — the very generous S wave voltage seen in leads V2, V3, V4 in ECG #2 strongly suggests probable LVH by Cornell and/or Peguero criteria.
• As emphasized in my June, 20 Comment — in the presence of very deep anterior S waves — LV "strain" sometimes manifests in anterior leads as ST elevation with T wave peaking (ie, the "mirror-image" of lateral lead ST "strain" depression). This might account for the ST-T wave picture we see in leads V1-thru-V3 of ECG #2.
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• Hyperkalemia is another interacting factor. An elevated serum K+ = 6.1 mEq/L in a patient with acute renal insufficiency is certainly a high enough value to produce anterior lead T wave peaking (perhaps superimposed on already peaked anterior T waves from the "mirror-image" of LV "strain").
• So WHY aren't peaked T waves seen in more leads in ECG #2? One possible answer to this could be that the reason ST-T waves are so "flat" in all lateral leads in ECG #2 — is that preexisting ST depression from LV "strain" has attenuated T wave peaking from superimposed hyperkalemia.
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• BOTTOM LINE: I completely agree that the ECGs in today's case show no indication of acute coronary occlusion. But there are a number of interacting factors that may be superimposing or attenuating their effects on ECG. I think it important to appreciate that we will not know what the "true" ST-T waves look like in today's patient until the ECG is repeated after serum K+ is corrected.

Figure-3: The ECG criteria I favor for diagnosis of LVH (I've reproduced this Table from My Comment in the June 20, 2020 post in Dr. Smith's ECG Blog).