Chest pain with 2 serial ECGs, with dynamic change, texted to me

These were texted to me only with "chest pain."

First:

2nd:

What was my response?

Smith: Young thin black male.  No OMI.

Texter: Can't fool you.  It was indeed.  

Queen: #1: NOT OMI, HIGH CONFIDENCE

Queen: #2: NOT OMI, HIGH CONFIDENCE

ECG 1 Interpretation: there is terminal T-wave in V3-V6.  Is this Wellens' pattern A?  No. this is classic Benign T-wave Inversion.  It helps to know that the patient has active chest pain, as Wellen's is a post occlusion (reperfusion) state, with open artery and pain-free.

See 2 dozen examples here: 

Understanding this pathognomonic ECG would have greatly benefitted the patient.

ECG 2 Interpretation: Now the T-waves have become upright, so this must be re-occlusion  (pseudonormalization), right?  No.  It is still normal.  It is an unfortunate fact that benign T-wave inversion (and ANY T-wave inversion), AND ALSO early repolarization (normal variant STE) can be dynamic.

Outcome:

Patient ruled out for MI by troponins.

Here is a great case of pseudonormalization.     Here are multiple cases.

LEARNING POINT: 

1. Morphology matters.  Pattern recognition is essential.  AI does a great job at this but most humans do not.  

2. And ECGs can change and evolve even when there is no ischemia.  This is where morphology is most critical!

And so: 

I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:

The Queen is taught be pattern recognition, not by any rules.  We just give it ECGs and tell it what they represent.  After "seeing" thousands and thousands of them, it can recognize the patterns just like we humans (and AI!) can recognize faces.

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MY Comment, by KEN GRAUER, MD (6/30/2023): 

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Today's case provides an excellent example of how appreciation of pattern recognition facilitates distinction between ECG findings indicative of an acute evolving event vs a benign variant.

• As per Dr. Smith — the already uncanny accuracy of the QoH (Queen Of Hearts) AI application program for identifying acute OMI, is a result of a data base input provided by Drs. Smith and Meyers containing thousands of tracings with documentation of cardiac catheterization results. But the clinical need — is to improve the ECG interpretation ability of the majority of emergency care providers who do not have this extensive ECG-cath-result data base experience to fall back on.

Along the way to acquiring more experience in recognizing the ECG findings of acute coronary occlusion — is incorporation of a number of KEY ECG Features into one's clinical acumen.

• For clarity in Figure-1 — I've reproduced and put together the 2 serial ECGs that were texted to Dr. Smith in today's case.

Figure-1: Comparison between the 2 ECGs in today's case that were texted to Dr. Smith. (To improve visualization — I've digitized the original ECG using PMcardio).

KEY ECG Features:

As per Dr. Smith — ECG #1 manifests the classic features of BTWI (Benign T Wave Inversion). To the "uninitiated" — this 1st ECG that was texted to Dr. Smith shows ST elevation in each of the chest leads — with T wave inversion in leads V3-thru-V6. That said — ECG #1 satisfies almost all of the 9 Criteria derived over the years by Drs. Wang and Smith as suggestive of BTWI (These criteria were cited by Dr. Meyers in the March 22, 2022 post of Dr. Smith's ECG Blog). With experience — recognition of these criteria becomes automatic — but until that experiential point is attained, referral to the following bulleted list of these 9 Criteria may prove invaluable:

• Criterion #1: There is a relatively short QT interval (which I estimate at <400 msec. in ECG #1).
• Criterion #2: The leads with T-wave inversion often have very distinct J-waves (prominent J-point notching being seen in leads V3-thru-V6 in ECG #1).
• Criterion #3: The T-wave inversion is usually in leads V3-V6 — which is in contrast to Wellens' syndrome, in which T-wave inversion is usually in leads V2-V4 (T-wave inversion being seen in leads V3-thru-V6 in ECG #1).
• Criterion #4: The T-wave inversion does not evolve and is generally stable over time — which is in contrast to Wellens' Syndrome, which always evolves. (and although ST-T wave morphology does change in several leads from ECG #1 to #2 — this is not really in a true "evolution" pattern).
• Criterion #5: Chest leads with T-wave inversion often have some ST elevation (This is especially well seen in leads V3,V4,V5 of ECG #1).
• Criterion #6: Right chest leads often have ST elevation typical of classic early repolarization (This is especially noted in lead V2 in ECG #1 — in which the upward concavity = "smiley"-configuration shape of the ST elevation is typical for a repolarization variant).
• Criterion #7: The T-wave inversion in leads V4-V6 is preceded by minimal S-waves (There are no S waves in leads V4-6 of ECG #1).
• Criterion #8: The T-wave inversion in lateral chest leads V4-V6 is preceded by high R-wave amplitude (R waves in leads V4-V6 are ≥20 mm).
• Criterion #9: Leads II, III, and aVF also frequently have T-wave inversion (This is the 1 criterion not satisfied in ECG #1).

Additional benign-appearing features in ECG #1 — include: i) Lack of pathologic Q waves (the tiny ones that are seen, are normal septal q waves that appear in several of the lateral leads); — ii) There is no reciprocal ST depression; — and, iii) The very similar-looking upward concavity ("smiley"-configuration) ST elevation, with distinct J-point notching and T wave inversion — is seen in no less than 4 consecutive leads. It is quite unusual for acute evolving OMI to manifest such a similar ST-T wave picture in this many consecutive leads.

ECG #2 shows a CHANGE in ST-T Wave Appearance:

As per Dr. Smith — the ST-T wave appearance in benign repolarization patterns is not always constant. Instead, the ST-T wave appearance may change in serial tracings recorded over the course of a single ED visit. Although this is not a common phenomenon — You will see it on occasion (See the July 24, 2013 post, among others — in Dr. Smith's ECG Blog). As might be imagined — the potential for the ST-T wave appearance of benign repolarization patterns to vary can be easily confused with "dynamic" ECG changes indicative of an acute evolving OMI.

• Greenfield and Rembert have noted that up to 1/3 of patients with ER (Early Repolarization) but no cardiac symptoms — may show marked variation in the amount of ST elevation from one tracing to the next. These ER patients do not have ischemia — and the variation in ST elevation has not been shown to be related to either heart rate or QRS amplitudes (Variation in ST-Segment Elevation in Early Repolarization: Electrocardiography 40:10,2007).
• 
  
• In ECG #2 — 4 leads show a change in ST-T wave appearance. This variation entails: i) Straightening of the ST segment in lead V3, with loss of T wave inversion in this lead; ii) Increased ST elevation in lead V4, albeit with loss of R wave amplitude in this lead; and, iii) Loss of T wave inversion in leads V4-6.
• 
  
• That said, my overall impression of ECG #2 — was that this variation just did not "look" like a true "dynamic" ST-T wave change indicative of an acutely evolving OMI because: i) Prominent J-point notching persists in the 4 leads with ST-T wave changes in ECG #2; ii) The QTc interval remains relatively short in ECG #2 — with a similar-looking, upward concavity ST segment shape that persists in each of the lateral chest leads; and, iii) There is no significant ST-T wave change in any of the other 8 leads.
• 
  
• NOTE: If the change in ST-T wave appearance in today's 2 serial tracings represented true "dynamic" variation in an acutely evolving OMI — then I would expect the T wave inversion in leads V3-thru-V6 of ECG #1 to represent reperfusion T waves — with loss of this T wave inversion and the increase in ST elevation seen in ECG #2 to represent acute reocclusion. But in the absence of a clear increase in CP (Chest Pain) severity in association with ECG #2 — I would attribute the change in ST-T wave appearance to the variation that may sometimes be seen with repolarization patterns. 

Young Man with Very Fast Regular Wide Complex Tachycardia

EMS was dispatched for a 30-something male who feels his heart is racing.  Sudden onset.

The patient had no previous medical history.

Vitals were normal except for a heart rate of 226.

A prehospital 12-lead was recorded:

There is a regular wide complex tachycardia.  The computer diagnosed this as Ventricular Tachycardia.

Is it definitely VT??

The patient was given 6mg, then 12 mg, of adenosine, without a change in the rhythm.

He arrived in the ED and had an immediate bedside cardiac ultrasound while this ECG was being recorded.

The bedside ultrasound (video not available) reportedly showed only a slightly reduced LV function.

Here is the ECG:

What do you think?

There is a wide complex regular tachycardia at a rate of 226.  The first part of the QRS is slow onset (see magnification below).  The differential is VT vs. AVRT.  

Could it be RVOT (Right ventricular outflow tract VT).  No, this requires inferior axis and LBBB morphology.  There is no inferior axis.

RVOT VT:

A 40-something without past history presents with wide complex tachycardia and crushing chest pain

 

Regular Wide Complex Tachycardia. What is the Diagnosis?

Toothache, incidental Wide Complex Tachycardia

Could it be fascicular VT or Bundle Branch VT (i.e., idiopathic VT)?   No, because the first part of the QRS is slow onset (see magnified V1-V6 below).

Could it be standard VT?  Yes, but this would be unusual in someone with no cardiac history and a reasonably good contractility on echo.

Could it be AVRT?  Yes.

If AVRT, adenosine is likely to work, but it did not work in the prehospital setting.  

Perhaps:

1) it is VT 

2) the dose of adenosine was too low or

3) the adenosine was not given fast enough.

V1-V6 magnified, with lines marking onset of QRS and end of first part of QRS:

From the onset of the QRS to the nadir of the S-wave is greater than 100 ms, which is not consistent with a SVT with aberrancy or with VT that is initiated in conducting fibers (idiopathic VT such as posterior fascicular VT or BBB VT).

Thus, this is more likely:

1) antidromic AVRT (down through accessoary pathway and up through the AV node OR

2) standard VT which begins in myocardium and thus has a wider initial part of the QRS.

Case continued.

The patient was immediately electrically cardioverted.

Here is the post cardioversion ECG:

What do you think?

The initial ECG could be either VT or Antidromic AV Reciprocating Tachycardia (using an accessary pathway -- in other words, WPW).

Does a post cardioversion ECG without delta waves rule out WPW?

No.  Some people with accessory pathways do not have delta waves at baseline, some have them only sometimes, some delta waves are so intermittent that the same ECG will have some beats with delta waves and some without.  

Example: What do you think of this "Ventricular Bigeminy"?

  

The absence of delta waves is sometimes called "Concealed conduction", though this term has fallen out of favor.  See here about concealed conduction.

Wide Complex Tachycardia, and What is Latent Conduction and "Concealed Conduction?"

20-something with anxiety. Pulse is 169. Then 229. Then 169. Then 229. Latent conduction vs. Concealed Conduction. 3 Pathways.

Was it a good idea to try adenosine?

Yes.  A regular wide complex tachycardia in a young patient with no history of heart disease is very likely to be AVRT.   VT is not harmed by adenosine,

When is adenosine dangerous?

It is dangerous in WPW with atrial fibrillation.  It is NOT dangerous when the tachycardia is regular.  In Atrial Fibrillation, the tachycardia will always be irregularly irregular.  In Atrial fib with WPW, there will be polymorphic QRS complexes (in this case, all QRS complexes are identical).  There would also be some R-R intervals that are VERY short (less than 240 ms).

Case Continued

He underwent an MRI to look for scar as a nidus for VT:

IMPRESSION
1) Borderline LV function with no focal wall motion abnormalities
2) Normal dimensions of all cardiac chambers
3) No evidence of myocardial scar on delayed enhancement sequences after contrast administration
4) No MRI evidence of arrhythmogenic right ventricular dysplasia.

EP note:

"He had wide-complex monomorphic tachycardia with extreme axis concerning for VT. He is young and the tachycardia was not polymorphic in nature, so this is very unlikely to be an ischemic rhythm and much more likely scar mediated. He got an MR, however that showed no scar or evidence of AVRD and he had a stress test with no evidence of inducible ischemia with almost 20 METs." 

 

He underwent an EP study 5/10/2022 for evaluation of pre-excitation/accessory tract which found a left sided accessory pathway - he is currently in the EP study now. Cardiology consults will continue to follow in the morning and address necessary cardiology follow-up. 

 

EP study confirmed an accessory pathway.  It was ablated.

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MY Comment, by KEN GRAUER, MD (6/28/2023):

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There is a tendency for clinicians to interpret cardiac arrhythmias in binary fashion. By this I mean — that a given rhythm is interpreted as being either Diagnosis #1 or Diagnosis #2, with "nothing" in between. Clinically — this most often this relates to a rhythm being interpreted as either VT or SVT.

• In my opinion — it is a mistake to interpret arrhythmias in strict "binary" fashion — since rather than "either/or" — optimal interpretation is more of a probability statement.

To illustrate this concept — I've reproduced in Figure-1, the initial ECG recorded on today's patient in the ED.

• Rather than calling this rhythm "definitely" VT — optimal interpretation would entail description of this rhythm as a regular WCT ( = Wide-Complex Tachycardia) at ~225-230/minute, without clear sign of atrial activity.  

KEY Point: The principal differential diagnosis of a regular WCT rhythm without clear sign of atrial activity includes: i) VT (which statistically in an unselected adult population makes up at least 80% of cases); ii) Some type of SVT with either preexisting BBB or aberrant conduction; — or — iii) Something else (with this "something else" including entities such as hyperkalemia and/or WPW-related tachyarrhythmias).

• The above statistics are derived from an unselected adult population. Additional factors may help greatly to narrow down and increase relative probability of one or another diagnosis.
• For example — in an adult of a "certain age" (ie, a patient beyond the "young adult" age range — usually beginning near "middle-age") — IF the patient has underlying heart disease — then even before looking at the actual ECG, statistical odds that a regular WCT rhythm without sign of atrial activity will turn out to be VT approach 90%.
• Use of QRS morphology may help to further increase the accuracy of this prediction. For example, IF this patient were an adult of a "certain age" who had known underlying heart disease — the fact that the QRS complex during the WCT rhythm in Figure-1 is extremely wide — with an amorphous QRS complex in all anterior leads, in which there is very slow initial depolarization — with predominant negativity of the QRS in lead V6 — and — with a QRS morphology that fails to resemble any form of known conduction defect — would suggest >95-98% likelihood that this WCT rhythm was VT.

The above said — today's patient was not an older adult with known heart disease. Instead — today's patient was a previously healthy man in his 30s.

• Not commonly appreciated is how surprisingly common VT may be in younger adult patients who present with a regular WCT rhythm without clear sign of P waves. That said — such patients almost always have idiopathic VT, in which there is no underlying heart disease!
• I've reproduced in Figure-2 — the KEY features of QRS morphology characteristic of some form of idiopathic VT. These generally entail fascicular VT (most commonly manifesting RBBB-LAHB or RBBB-LPHB-like morphology) or RVOT VT (recognized by LBBB-like morphology in the chest leads with an inferior frontal plane axis). The marked QRS widening, with amorphous shape in anterior leads seen in today's tracing is clearly not suggestive of idiopathic VT. 
• 
  
• BOTTOM Line: As per Dr. Smith — the fact that today's patient was a previously healthy young adult who presents with the markedly abnormal QRS morphology seen in the WCT shown in Figure-1 — dramatically reduces the likelihood of VT (especially given no sign of anatomic cardiomyopathy on bedside ultrasound!).

Figure-1: The initial ECG that was recorded in the ED.

Final PEARL:

Although the differential diagnosis of an SVT with a wide QRS includes sinus tachycardia (with either preexisting BBB or aberrant conduction) and AFlutter — the rate of ECG #2 in Figure-1 ( = ~225-230/minute) — is too fast for sinus tachycardia in an adult — and "off" for either 1:1 or 2:1 AFlutter (in which the atrial rate of untreated flutter is typically between 250-350/minute).

• As per Dr. Smith — this establishes AVRT as the principal diagnostic consideration. The overwhelming majority of AVRT reentry SVTs are conducted "orthodromic" (ie, passing first down the normal AV nodal pathway — thereby resulting in a narrow QRS complex).
• That said — from 1-to-5% of reentry AVRT rhythms are "antidromic", in which the reentry circuit passes first down the AP (Accessory Pathway) — which results in a wide QRS. Antidromic AVRT is precisely the mechanism for the overly wide and unusual QRS morphology seen in today's case!
• There is a tendency to assume that regular WCT rhythms without atrial activity are VT. While true in >95% of cases — it is well to keep in mind that on occasion (especially in a previously healthy younger adult) — we may see a regular WCT due to antidromic AVRT. Distinctinction between antidromic AVRT and VT may not be possible from the single ECG obtained during the WCT rhythm (as was the case today!).

Figure-2: Review of the KEY features regarding Idiopathic VT (which I previously published in My Comment at the bottom of the page in the May 14, 2022 post in Dr. Smith's ECG Blog). 

An Intriguing Rhythm: Who Belongs to Whom?

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MY Comment, by KEN GRAUER, MD (6/26/2023): 

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The tracing in Figure-1 was sent to me — without the benefit of any history. How would YOU interpret this tracing?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Initial Thoughts:

My attention was immediately drawn to the long lead rhythm strip in Figure-1. A lot is going on ...

• The rhythm is clearly irregular. 
• All QRS complexes in this tracing are narrow — so the rhythm is supraventricular.
• P waves are present — and there is more than 1 P wave shape.
• Some P waves are too close to the QRS to conduct. That said, on initial inspection — it's hard to determine, "Who belongs to whom?" 

My Approach:

When confronted with a challenging tracing consisting of multiple components, such as we see in Figure-1 — I favor starting with parts of the rhythm that I am fairly certain about.

• I find that the simple act of labeling atrial activity is incredibly helpful. In Figure-2 — I've added RED arrows to the long lead rhythm strip in today's initial tracing to highlight what appears to be sinus P waves.
• 
  
• Now look at each of these RED-arrow P waves. Which of these P waves do we know will be unable to conduct (because the PR interval until the next QRS complex is just too short?).
• It should be apparent that the PR interval in front of beats #3,4; 9; 14 and 15 is too short to conduct! Since the QRS complex for each of these non-sinus-conducted beats is narrow — beats #3,4; 9; 14 and 15 must be junctional beats.
• 
  
• PEARL #1: IF the R-R interval that contains an on-time P wave is shorter-than-expected — this is a strong clue that suggests the reason the R-R interval unexpectedly shortens, is that this P wave is being conducted. For example, in Figure-2 — Notice how the R-R interval clearly shortens before beats #6 and 11 (ie, from at least 780 msec. — to 710 and 720 msec., respectively). This strongly suggests that beats #7 and 11 are sinus-conducted!
• 
  
• PEARL #2: The R-R interval before each of the junctional beats in Figure-2 is between 780-to-800 msec. This corresponds to a junctional rate of ~80-85/minute — which means that there is an accelerated junctional rhythm in today's tracing, that is periodically interrupted when the rate of SA Node discharge increases enough to "take over" command of the rhythm (ie, which happens with sinus-conducted beats #6 and 11).
• 
  
• NOTE: It is unclear if beat #5 is junctional or sinus-conducted. Although I suspect beat #5 is sinus-conducted (because it manifests the same PR interval as beat #6, which we know is sinus-conducted) — this does not matter clinically, because regardless of the etiology of beat #5 — today's tracing still manifests an accelerated junctional rhythm that is periodically interrupted by sinus-conducted beats.

Figure-2: I've added RED arrows to the long lead II rhythm strip from Figure-1 to highlight sinus P waves. Which of these P waves are unable to conduct?

What About the Remaining Beats?

In Figure-3 — I've added YELLOW arrows over each of the remaining P waves. These YELLOW arrows highlight the 5 PACs (Premature Atrial Contractions) in today's tracing — which are recognized as PACs, because beats #2; 7,8; and 12,13 all occur earlier-than-expected — and — are preceded by P waves with an obviously different morphology compared to the sinus P waves under the RED arrows.

• BOTTOM Line: Even without calipers — We've been able to rapidly establish that today's rhythm consists of an underlying sinus rhythm — that is punctuated by PACs, and intermittently interrupted by an accelerated junctional rhythm.
• 
  
• PEARL #3: There is transient AV dissociation in today's tracing — because a number of the sinus P waves that we see in Figure-3 are not related to neighboring QRS complexes. As I discuss in detail in My Comment at the bottom of the page in the May 24, 2020 post in Dr. Smith's ECG Blog — AV dissociation is not the same as AV block. The fact that none of the P waves in Figure-3 that fail to conduct have a realistic chance to conduct (because the PR interval before beats #3,4; 9; and 14,15 is too short to conduct!) — suggests that there may be no AV block at all in today's tracing.
• 
  
• PEARL #4: The fact that the sinus P wave rate and the accelerated junctional rate in today's tracing is very similar, such that control of the rhythm alternates between the SA and AV nodes — suggests that today's rhythm represents isorhythmic AV dissociation (this concept also discussed more in my May 24, 2020 comment).
• 
  
• PEARL #5: Accelerated junctional rhythms are not common in adults. Most occurrences are associated with events such as sepsis, shock, recent infarction, post-operative state, electrolyte disturbance — or "sick patient". This led me to wonder what the clinical situation in today's case might be!

Figure-3: I've added YELLOW arrows to Figure-2 to highlight that morphology for the P waves that precede beats #2; 7,8; and 12,13 is different than P wave morphology highlighted by each of the RED arrows.

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Clinical Follow-Up in Today's CASE:

It turns out that the clinical history in today's case was that of a patient with overuse of illicit drugs — who was assaulted, suffering severe trauma. Seizure activity was witnessed at the scene — and head CT scan showed a small bleed.

• The patient's severe medical condition therefore provided a clinical setting potentially predisposing to the above described arrhythmia (with the accelerated junctional rhythm).

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LADDERGRAM Illustration:

A picture is worth 1,000 words. I've drawn in Figure-4 my proposed laddergram illustration for today's case. (IF interested in learning more on how to read and/or draw laddergrams — CLICK HERE).

• According to the laddergram — beats #5,6 and 11 are sinus-conducted (showing normal conduction through the Atria, A-V Nodal and Ventricular Tiers).
• Beats #2; 7,8; and 12,13 are PACs (showing different P wave morphology, as highlighted by YELLOW arrows). PACs originate from a non-sinus node site in the atria — and then conduct normally to the ventricles after passing through the AV node.
• Beats #3,4; 9,10; 14,15 represent an accelerated junctional focus (RED circles showing origin of impulse formation within the AV Nodal Tier). Retrograde conduction from these junctional beats (dotted RED lines) blocks forward conduction of the on-time sinus P waves with a short PR interval.

Figure-4: My proposed laddergram for today's rhythm.

One More Tracing in Today's CASE:

I was able to obtain an additional 12-lead ECG and rhythm strip from today's case — which is shown in Figure-5. This additional tracing (TOP panel in Figure-5) — is the original ECG that was done in the ED on today's patient. 

CHALLENGE Question:

• Why do we not see the accelerated junctional rhythm in ECG #2?

Figure-5: Compare the rhythm in the initial ECG obtained in the ED (TOP) — with the BOTTOM rhythm strip, that I showed in Figure-3. Why do we not see the accelerated junctional in ECG #2?

ANSWER to the Challenge Question:

Note that the rhythm in ECG #2 is sinus tachycardia at ~100-105/minute. Thus, the atrial rate in ECG #2 is faster than the atrial rate of sinus P waves in the BOTTOM rhythm strip.

• Although the junctional rhythm that we saw intermittently in today's tracing was accelerated (to ~80-85/minute) — this junctional rhythm never attains as rapid a rate as the sinus tachycardia seen in ECG #2. As a result — we don't see the junctional rhythm in ECG #2.
• 
  
• P.S.: I conclude today's case by commenting on the other leads in the 12-lead tracings. QRS voltage looked increased in both tracings (though depending on the age of the patient — this may not necessarily qualify as voltage for LVH). The frontal plane axis was vertical in ECG #2 (and slightly rightward in ECG #1). There are nonspecific ST-T wave changes — but no indication of an acute cardiac event.

Wide complex tachycardia and hypotension in a 50-something with h/o cardiomyopathy -- what is it?

A 50-something male with unspecified history of cardiomyopathy presented in diabetic ketoacidosis (without significant hyperkalemia) with a wide complex tachycardia and hypotension.

Bedside echo showed "mildly reduced" LV EF.

Here is the ED ECG:

What do you think?

Analysis: there is a wide complex tachycardia. It is regular.  There are no P-waves.  The morphology is of RBBB and LAFB.  The initial part of the QRS is very fast, suggesting that it starts in conducting fibers and not in myocardium.  Thus, it is probably SVT with aberrancy (RBBB + LAFB) or it is posterior fascicular VT (which starts in the posterior fascicle and therefore also has a fast initial depolarization nearly identical to RBBB + LAFB).

The fact that he has a cardiomyopathy argues for a more typical ventricular tachycardia, as does the absence of rSR' in lead V1.  One of the Brugada criteria is RBBB pattern but with the firsr R-wave being larger than the 2nd (true RBBB has rSR' -- that is, the first r- is small and the 2nd R- is large).

The providers for this patient did not spend a lot of time trying to figure this out.  Because the patient was critically ill, they just went ahead and sedated and cardioverted.  

They probably would have had time to give adenosine (after all, they had time to draw up sedatives prior to electrical cardioversion).  Adenosine is safe even if it is VT.  If it is posterior fascicular VT, then verapamil works, but that is very risky in a patient with hypotension.

Here is the difference between VT RBBB and normal RBBB:

In spite of this slightly abnormal morphology, the most important aspect by far that differentiates this from typical VT is that the initial portion of the QRS is fast.  

(The less common atypical VT, otherwise known as idiopathic VT, acts more like SVT with aberrancy because it uses conduction fibers.)

Let's look more closely, magnified:

Click on the image to see it in full size.

I have placed for each lead a line that is at the beginning of the QRS (the left line, with the right side of that line directly at the start of the QRS) and then the 2nd line has its left side at the end of the RS or QR, which is the first part of the QRS.

You can see that that first part of the QRS is about 50 ms.  This is very fast.  

LBBB and RBBB have comparable initial deflection duration.

LBBB has R/S less than 70 ms

RBBB is shorter still.

This was the interpretation I put into the system: 

WIDE COMPLEX TACHYCARDIA.

Has fast early component, with RBBB and LAFB. Thus, possible SVT with RBBB/LAFB or posterior fascicular VT

More typical VT is also possible, as the RBBB is atypical (Brugada criterion): first R-wave is larger than 2nd R-wave in V1

MARKED ST DEPRESSION, SUBENDOCARDIAL ISCHEMIA 

Here is the post cardioversion ECG:

See lead II across the bottom: There are either down-up T-waves, or inverted T-wave followed immediately by a P-wave and prolonged PR interval.  In V1, there is a negative deflection that could be the normal negative component of the P-wave in V1, but it might not be.  I was not certain if this was a fast junctional rhythm or if it was sinus tach, so I wrote: 

UNCERTAIN REGULAR SUPRAVENTRICULAR RHYTHM

RIGHT AXIS DEVIATION  [QRS AXIS > 100]

RIGHT BUNDLE BRANCH BLOCK

The patient had another episode of wide complex tachycardia and was electrically cardioverted again.  He was started on amiodarone and had no more events.

Next day, the cardiologists were convinced (I think correctly) that this was SVT with aberrancy that was triggered by DKA.

The patient later settled into sinus bradycardia.

The amiodarone was discontinued and the patient did well.

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MY Comment, by KEN GRAUER, MD (6/23/2023):

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From an academic standpoint — I love WCT (Wide-Complex Tachycardia) rhythms. That said — from a clinical standpoint regarding initial ED management, the intricacies of determining the etiology of the various WCT rhythms is far less important that "treating the patient" (ie, If the patient is at all hemodynamically unstable or otherwise in precarious clinical condition — immediate synchronized cardioversion will be indicated regardless of whether the rhythm is VT, some type of SVT — and/or a WPW-related tachyarrhythmia).

• The above said — Dr. Smith's approach to today's arrhythmia highlights a number of important points! I focus my comments on some additional thoughts that add to his excellent discussion.

For clarity in Figure-1 — I've reproduced and labeled the 2 ECGs in today's case.

Figure-1: I've labeled the 2 ECGs in today's case (See text).

MY Thoughts to Today's Initial ECG:

In the BEST of hands — prediction of the etiology of a regular WCT rhythm is less than perfect. Sometimes, it isn't very good at all. But at other times — we can be surprisingly accurate in predicting the etiology of a regular WCT rhythm by considering a number of clinical features.

• I've reviewed "My Take" on distinction between VT vs some form of SVT with either rate-related aberrant conduction or preexisting bundle branch block on many occasions in My Comments at the bottom of the page in Dr. Smith's ECG Blog (ie, in the August 13, 2020 post — the June 25, 2020 post — the April 23, 2019 post — and the April 15, 2020 post, to name just a few).
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• To Emphasize: The fact that today's patient was acutely ill with DKA and hypotensive in association with the initial ECG shown in Figure-1 — meant that immediate synchronized cardioversion (as was done) was the treatment intervention of choice regardless of what the etiology of his regular WCT turned out to be!

Statistics:

• It's important to appreciate that statistical odds that in an unselected population of adults of a certain age — at least 80% of regular WCT rhythms without clear sign of atrial activity will turn out to be VT. This likelihood of VT increases to at least 90% if the patient has documented underlying heart disease. Given the presence of significant diabetes (severe enough to present with DKA) and known cardiomyopathy — this means that even before looking at the ECG, today's patient presented with a ≥90% likelihood that ECG #1 would turn out to be VT.
• As a result — the "onus of proof" is on us to show that the initial ECG is not VT, rather than the other way around. With a patient such as the one in today's case — Assume VT until proven otherwise, and treat accordingly.
• Just because a regular WCT is VT does not necessarily mandate immediate cardioversion — IF the patient is hemodynamically stable and tolerating the arrhythmia. Today's patient was not stable — so cardioversion was immediately undertaken, with successful conversion to a much narrower (presumably supraventricular) rhythm, as shown in ECG #2.

Other Clinical Factors?

• Today's patient presented with a wide tachycardia and DKA. Although his initial ECG does not look like the ECG of a patient with hyperkalemia — serum K+ should be immediately assessed given lack of atrial activity and QRS widening in a patient with DKA.

QRS Morphology:

I interpreted the rhythm in ECG #1 — as a regular WCT at ~170/minute, without clear sign of atrial activity. Based on the appearance of ECG #1 — I initially thought this rhythm was VT. I did so because QRS morphology was not typical of any known form of conduction defection. Although there is superficial resemblance to rbbb/lahb conduction — there are many atypical features. These include: 

• Lack of a triphasic QRS pattern in lead V1, in which there is a distinct S wave that descends below the baseline — that is followed by a terminal "right rabbit ear" in the form of a relatively slender R' that is taller than the initial r wave in this lead. Instead, there is a taller "left rabbit ear" in lead V1 — which if anything, is more suggestive of VT than of supraventricular rbbb conduction.
• Although wide terminal S waves are seen in both lateral leads I and V6 — they are associated with extremely small r waves. This is atypical for supraventricular conduction (which most often manifests significantly taller lateral R wave forces in leads I and V6). 
• All 3 of the standard limb leads (ie, leads I, II and III) — manifest predominant negative deflections. This pattern is much more suggestive of fascicular VT than of supraventricular conduction.
• Small initial q waves are seen in both leads V2 and V3. This suggests either prior infarction — and/or — a ventricular etiology for the WCT rhythm.
• At 1st glance — the QRS complex in lead V1 appears to be extremely wide! This clearly did not look like a supraventricular etiology to me.

How Wide is the QRS in Lead V1?

Although I initially thought the QRS in lead V1 was extremely wide — as I contemplated a 2nd time (admittedly, in the comfort of my office chair in front of my large screen computer) — I thought the vertical RED line (that I drew in simultaneously-recorded leads V1,2,3 — extended downward to intersect in the long lead II rhythm strip) marked the true end of the QRS complex.

• If the vertical RED line that I drew in ECG #1 correctly marks the end of the QRS complex — then the elevated segment to the right of this RED line in lead V1 must represent ST elevation — which is only seen in lead V1. Could this ST elevation in only lead V1 represent Brugada Phenocopy in this patient with a regular WCT rhythm?
• To facilitate assessing where the QRS ends in the other 8 leads — I extended vertical PURPLE lines upward from the same landmark established by the vertical RED line in the long lead II complex under simultaneously-recorded leads V1,2,3.
• To Emphasize: Even if the QRS in lead V1 ends at the vertical RED line in this lead — I still thought overall QRS morphology in ECG #1 was atypical for supraventricular conduction for the other reasons I stated above. So, at this point in the case, on the basis of just ECG #1 — I thought the initial ECG rhythm had to be assumed VT until proven otherwise.

Is there a Preexisting ECG for Comparison?

When confronted with an acutely ill, hemodynamically unstable patient who presents with a regular WCT rhythm — there rarely is time to "pause" for search of a prior (baseline) ECG on the patient. But it is helpful to do so at the earliest reasonable opportunity — since on occasion, availability of a prior tracing on the patient may provide the answer!

• All bets are off when assessing a regular WCT rhythm in a patient with a markedly abnormal baseline ECG during sinus rhythm. In such cases — none of the "general rules" for QRS morphology used for distinction between SVT vs VT may hold.
• Unfortunately — NO prior tracing is provided in today's case. Instead — all we have is the post-conversion ECG ( = ECG #2 in Figure-1) — which shows that the QRS has narrowed (to between 0.10-to-0.11 second) compared to ECG #1 — but which (as per Dr. Smith) — fails to clearly show sinus P waves. 
• Presumably — ECG #2 is a supraventricular rhythm (either junctional tachycardia or sinus tachycardia with a long 1st-degree AV block) — in which the atypical features of incomplete RBBB conduction are the result of scar from prior infarction (ie, producing overall low voltage — Q waves in leads V2,V3 — and QRS fragmentation in a number of leads).

WHY Did the Post-Conversion Tracing Change My Mind?

After seeing ECG #2 — my impression of the initial ECG changed.

• As per Dr. Smith — the initial portion of the QRS complex in ECG #1 is relatively narrow (implying fast initial conduction — that is typical of a supraventricular etiology). More than this — the shape of the initial QRS deflection is virtually the same in most leads for ECGs #1 and #2.
• I've drawn vertical BLUE lines in both of today's tracings that define the initial portion of the QRS deflection that I am referring to. For example — the direction and slope to the LEFT of the vertical BLUE line in simultaneously-recorded leads I,II,III in both ECGs #1 and #2 show a similar tiny R wave in lead I — and a small, thin initial r with deep and steep S wave downslope in leads II and III.
• Similarity in the portion of the QRS to the LEFT of the vertical BLUE line in the other 9 leads in both tracings is likewise present. This high degree of similarity in the initial deflections of so many leads would be highly unlikely if ECG #1 was VT.

Learning Points:

• The accuracy of ECG criteria for prediction of VT vs SVT with either aberrant conduction or preexisting BBB is imperfect. Certain predictive criteria can be highly accurate. That said — today's case was especially challenging because: i) QRS morphology in the initial ECG was not optimally consistent with any known conduction defect; and, ii) The post-conversion tracing still showed atypical QRS morphology (ie, completely positive QRS in lead V1 — anterior Q waves — marked fragmentation).
• Initial management of an unstable patient in a regular WCT rhythm is the same regardless of whether the etiology of the rhythm is VT or an SVT = immediate cardioversion!
• Even though initial management of the unstable patient in a WCT is the same for both SVT and VT — determining the etiology of the initial rhythm may be extremely helpful for deciding on further management (ie, For deciding which medication to continue the patient on after successful cardioversion, so as to prevent recurrence? — and at times for deciding whether or not to refer the patient to EP cardiology, which may depend on what the diagnosis of what the WCT was).
• Finding a prior ECG on the patient may prove invaluable — especially for comparaing QRS morphology during the WCT rhythm compared to the patient's baseline ECG during sinus rhythm.
• RBBB conduction produces a terminal delay in QRS morphology. The fact that the initial QRS deflection in virtually all leads of today's tracing was both narrow and virtually identical in direction and slope (ie, the deflections to the LEFT of the vertical BLUE lines) — supports a supraventricular etiology for the WCT in today's case.
• Other factors may alter QRS morphology of a supraventricular rhythm (ie, hyperkalemia, transient development of a Brugada Phenocopy pattern).
• Certain fascicular VTs may manifest a QRS morphology that is consistent with rbbb/lahb conduction. That said — I agree with Dr. Smith that the initial ecg in today's case more likely than not was supraventricular in etiology.
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• I wish we could find a baseline tracing on today's patient for comparison ...