A 30-something with acute chest pain

This was sent to me from Sam Ghali (@EM_Resus) with no other information.  I assumed it was a patient with acute chest pain.

"What do you think, Steve?  Real or just fake?"

What do YOU think?

It has some inferior ST elevation with some reciprocal ST depression and inverted T in aVL.  This usually indicates inferior OMI.

My answer: "Fake: pretty certain, but not 100% certain."

Sam: "why do you say fake?"

Smith: "Gestalt, but if I must explain: well formed J-waves and high voltage R waves."

Sam: "Yeah I think too the negative QRS in aVL takes away from changes that may be interpreted as “reciprocal”"

Smith: "did the cath lab get activated?"

Sam: "Yes, this case was sent to me.  It was a man in his 30s with chest pain.  Coronaries were clean.  Troponins were all negative -- the patient ruled out for acute MI."

Finally, Sam: "Honestly in addition to expert ECG interpretation I think skilled bedside echo can prevent a lot of these activations."

I agree, however: 

1) I don't think you can get a good enough echo without bubble contrast.  

2) You need to be just as expert at echo as I am at the ECG.

3) Echo is another step that takes time.  Time is myocardium.

So the best course of action:

 Use the PMCardio Queen of Hearts AI in ECG interpretation.

Not OMI with High Confidence

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We showed that the Queen of Hearts decreases false positive cath lab activations:

1) Published recently in Prehospital Emergency Care

Baker PO et al. Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study

This showed a decrease of false positive cath lab activations from 69 by medics to 29 by use of the Queen of Hearts, while still identifying all 48 true positive OMI.   I had only 9 false positives but I missed 2 OMI.  The integrated device algorithm had 42 false positives and one missed OMI.

Full text!

2) To be presented at AHA conference in Chicago in 2 weeks: 

Sharkey SW et al.  Performance of Artificial Intelligence Powered ECG Analysis in Suspected ST-Segment Elevation Myocardial Infarction.  This showed a decrease in false positive cath lab activations from 637 out of 2526 (25%) to 403 our of 2526 (16%), a 37% decrease in false positive activations.  Of those with MI and a culprit, 4% were missed (called "Not OMI"), but these were not necessarily occlusions (most MI with an open artery have a culprit), and many were LBBB.

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MY Comment, by KEN GRAUER, MD (10/3/2024):  

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I looked at the ECG in today’s case knowing only that the patient was a younger male adult with CP (Chest Pain).

• While statistical likelihood of acute OMI is clearly lower in younger adults — nothing is ruled out by age alone (as per My Comment in the January 9, 2023 and December 5, 2023 posts in Dr. Smith's ECG Blog).
• Without knowing more about today’s case — I also thought (as did Dr. Smith) — that this ECG (that I’ve labeled in Figure-1) was likely to be a “fake”. 

ECG Features suggesting "Fake"

As per Dr. Sam Ghali (who sent us today's case) — serial Troponins were clearly indicated since the patient presented to the ED. These were all negative. I'd defer on the question of whether cardiac catheterization was needed by saying, "Ya gotta be there" — but there clearly are ECG features suggesting no OMI.

• The rhythm for the ECG in Figure-1 is sinus — with normal intervals and axis (mean QRS axis about +80 degrees). There is no chamber enlargement.
• One wonders about lead placement, given abrupt transition from the similar-looking predominantly negative QRS complexes in leads V1,V2 — to a nearly all-positive QRS by lead V3.

Regarding ST-T Waves:

• There clearly is ST elevation in each of the inferior leads. 
• I suspect the presence of T wave inversion in lead aVL increased concern about reciprocal ST-T wave changes — which must have been perceived as suggestive of acute inferior OMI, since cardiac catheterization was performed.

There is No Reciprocal ST-T Depression:
We have often referred to the almost "magical" mirror-image relationship for ST-T waves in leads III and aVL when there is acute inferior MI (See My Comment in the September 30, 2019 post in Dr. Smith's ECG Blog, as well as many others). That said — I would not interpret ST-T wave appearance in lead aVL of today's ECG as a "reciprocal" change.

• The T wave vector often follows closely behind the QRS vector. As a result — when the QRS is predominantly negative in lead aVL — then the T wave in this lead may also be negative as a normal finding. This is precisely what we see in ECG #1 — in which the frontal plane axis is +80 degrees (which is most probably the reason for the shallow T wave inversion highlighted by the BLUE arrow in this lead).
• Contrast this normal amount of T wave inversion seen within the BLUE rectangle in ECG #1 — with the disproportionately "bulky" T wave inversion seen within the RED insert of lead aVL that I've excerpted from the initial ECG of a different patient who was having an acute OMI (See My Comment in the September 27, 2024 post).
• Therefore — there is no reciprocal ST-T wave depression in today's case!

There is No Sign of Posterior OMI:
It is common to see indication of posterior OMI when (if) there is inferior OMI. Posterior OMI is typically diagnosed by the finding of chest lead ST depression that is maximal in leads V2, V3 and/or V4. We do not see this in ECG #1.

• As noted above — the similar-appearing QRST complex in leads V1,V2 — followed by abrupt transition to a predominantly positive QRS by lead V3 — suggests there may be an error with precordial electrode lead placement.
• That said — None of the chest leads show ST depression.
• While the absence of indication of posterior OMI does not rule out the possibility of acute inferior OMI — it does make this less likely.

There ARE Signs of a Repolarization Variant:

Among the many posts in which we've reviewed cases of repolarization variants — is the May 23, 2022 post. From this post:

• Among the most suggestive ECG features of a repolarization variant — is the presence of an end-QRS notch (J wave) — and/or — a "slur" on the downslope of a prominent R wave.
• Although subtle — J-point notching is seen in leads V4 and V5 of ECG #1 (within the dotted PURPLE circles in these leads).
• A "slur" is seen on the downslope of the R waves in leads II,III,aVF and V6 (GREEN arrows in these leads).
• 
  
• Finally — Not only are reciprocal changes absent in ECG #1 — but a similar shape to the ST segments is seen in multiple leads (ie, leads I,II,III; aVF; V3,4,5,6) — which is more characteristic of a repolarization variant (as opposed to the ST-T wave changes of acute OMI that more often localize).

BOTTOM Line in Today's CASE: While fully acknowledging that in a patient who presents to the ED with CP — "Ya gotta be there" to best determine how much evaluation is needed to rule an OMI in or out. That said — I thought the ECG in Figure-1 looked more like a "fake" than like an acute OMI.

• Negative serial Troponins were needed to rule out an acute event.
• Serial ECGs would be expected to show no evolution.
• A normal Echo obtained during CP would support this being a repolarization variant.
• If a final test was perceived as "needed" — perhaps a normal coronary CT angiogram could have helped to avoid cardiac catheterization.

Figure-1: I’ve labeled the initial ECG in today's case. The RED Insert for lead aVL is excerpted from My Comment in the September 27, 2024 post in Dr. Smith's ECG Blog (taken from the initial ECG in that Sept. 27 post).

 

VT in a Sick Patient? Paired with 2 old cases (see them at the bottom)

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MY Comment, by KEN GRAUER, MD (8/30/2024):  

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I was sent the ECG shown in Figure-1 — knowing only that the patient was being seen in the ED (Emergency Department).

• How would you interpret this tracing? 

Figure-1: The initial ECG in today's case.

MY Initial Thoughts:

In my experience — all-too-many emergency providers fail to appreciate the potential contribution that a brief (1-to-2 line) history may convey when interpreting arrhythmias. Common things are common — so knowing what you are looking for (as is often suggested by the history) — may help you to find the answer. Not initially knowing the history in today's case — I considered the following:

• The ECG in Figure-1 — shows a regular WCT (Wide-Complex Tachycardia), at ~150/minute — with some uncertainty about atrial activity.
• QRS morphology in the chest leads is consistent with RBBB conduction (rsR' in lead V1 — and the presence of a wide terminal S wave in lead V6). This suggested a supraventricular etiology.
• BUT — the unusual frontal plane axis (ie, with predominant negativity in both leads I and II) was not consistent with any form of hemiblock. This instead suggested the possibility of fascicular VT?
• A distinct, rounded upright deflection in lead II (RED arrows in Figure-2) — clearly suggested atrial activity (? sinus P waves?) — but the finding of a regular tachycardia at a ventricular rate close to 150/minute with uncertainty about atrial activity — should always suggest the possibility of AFlutter with 2:1 AV conduction (and one might convince oneself of such 2:1 AV activity by the deflections under the BLUE arrows in Figure-2).
• And — Are those upright deflections under the RED arrows in lead II truly sinus P waves? (when the usual negative P wave deflection of sinus tachycardia is nowhere to be found in lead V1)?

What do YOU think?

Figure-2: How have I labeled the initial tracing?

The ANSWER:

At this point in the case — I was provided with 2 additional pieces of information:

• #1 Informational: It turns out that the patient in today's case was critically ill with multisystem problems. Synchronized cardioversion @200J was attempted twice on the rhythm in ECG #1 — but this had no effect on the rhythm.
• #2 Informational: I was provided with a repeat ECG on this patient — which was recorded a bit after ECG #1, still in the ED (Bottom tracing in Figure-3).

QUESTIONS:

• How does the #1 informational point that gives us a brief relevant history (including the effect of a treatment intervention) — help to increase our diagnostic certainty about today's rhythm?
• After seeing ECG #2 — Can you explain: i) Why no negative P wave was seen in lead V1 of ECG #1? — and, ii) Why the frontal plane axis was so unusual in the initial ECG (ie, with predominant negativity in both leads I and II in ECG #1)?

Figure-3: Comparison between the 2 tracings in today's case.

ANSWERS:

• Common things are common. While of course possible for the rhythm in ECG #1 to be either AFlutter or fascicular VT — sinus tachycardia immediately becomes a much more likely possibility once we know that this patient is critically ill with multisystem disease.
• Proof that the rhythm all along was sinus tachycardia will almost certainly be found in review of serial telemetry tracings — because there will almost always be gradual (progressive) increase or decrease in the sinus tach heart rate as the patient's clinical condition gets better or worse.
• AFlutter especially — but also monomorphic VT — are both responsive rhythms to synchronized cardioversion. The fact that two 200J cardioversion attempts failed to change the rhythm essentially rules out both AFlutter and VT. This essentially rules in sinus tachycardia. (If the BLUE arrows in Figure-3 were truly flutter waves — then we should be able to see more precise 2:1 activity in other leads, but we do not).
• 
  
• The reason that no negative sinus P wave is seen in ECG #1 — is that we learn from ECG #2 that the sinus P wave of today's patient is positive in lead V1 (the RED arrow in lead V1 of ECG #2).
• Instead — the RED arrow in lead II of ECG #2 highlights the upright sinus P wave in this lead — that is in retrospect, similar in both shape and in PR interval to the upright sinus P wave deflections that were seen in virtually all 12 leads in ECG #1!
• 
  
• Finally — The reason for the unusual frontal plane axis in ECG #1 — is simply that this patient's apparent baseline tracing (which I presume is like ECG #2) — shows marked right axis (predominantly negative QRS in lead I of ECG #2). 
• Note that the RBBB pattern seen in ECG #1 is not present in the baseline tracing — so with the tachycardia, this patient developed rate-related RBBB aberration. This rate-related aberrancy pattern resolves as the rate of this patient's sinus tachycardia is slowing (as it is in ECG #2).

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A Final Retrospective Look at the Initial ECG:

Among the most helpful tips for me toward improving my ability in arrhythmia interpretation — has been to retrospectively take another look at those tracings about which I was initially less than 100% certain.

• Although I suspected the deflections under the RED arrows in lead II of Figure-2 were sinus P waves — I initially considered other possibilities.
• In retrospect — the fact that these deflections are actually seen in no less than 10 of the 12 leads at the same point in the cardiac cycle is virtually definitive for sinus tachycardia!

To demonstrate this — We take advantage of the simultaneous recording of the long lead V1 rhythm strip with each of the 4 groups of 3 leads — as shown in Figure-4.

• I drew the vertical RED timeline in Figure-4 — to correspond to what looks to be the beginning of the P wave in lead II. Note where this vertical RED line passes in simultaneously-recorded leads I, III — and especially in the long lead V1 rhythm strip (where this RED line corresponds to the point just before a tiny positive deflection in this V1 lead).
• I then drew in the vertical BLUE timeline — to correspond to what looks to be the end of the P wave in lead II. Doing so defines a biphasic (tiny positive — then tiny negative) P wave in lead V1, which is consistent with the sinus P wave morphology that is commonly seen in lead V1.
• I then carried over the point in the long lead V1 that corresponds to the beginning of the tiny positive deflection in this lead — extending a dotted PURPLE line upward through the corresponding point in the other 9 simultaneously-recorded leads. Doing so identifies the precise beginning point of the small positive deflection that we see in all leads except aVR and aVL.
• Neither VT nor AFlutter will so consistently show the onset of a small, upright deflection at the identical distance before the next QRS complex in 10 of 12 leads. In Retrospect: This finding could have allowed me to be certain these positive deflections that are seen in 10 of 12 leads are P waves — and that the rhythm was sinus tachycardia.

Figure-4: I’ve added vertical timelines that correspond to P wave activity in 10 of the 12 leads.

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 — My appreciation to Sam Ghali (@EM_RESUS) for his contribution of today's case.

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Final Diagnosis:  

Sinus Tachycardia with Right Bundle Branch Block.

No evidence of OMI.

Other Cases of Sinus Tach with Wide Complex due to RBBB.  

These were catastrophically missed (EM cath lab activation cancelled both times by the interventionalist)

Here is a case of Sinus with RBBB and LAFB that was diagnosed correctly by the emergency physicians as acute STEMI.  The interventionalist was convinced it was VT without acute OMI.  So he would not cath the patient.  The patient died of cardiogenic shock:

Go to the post to see the full explanation.

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

This is a similar case of a 20-something year old woman, previously healthy, with acute pulmonary edema.  Her ECG was also dismissed and she died: