This was sent by a former resident, John Dunbar:

“Had this one the other day. 60s, no medical history but didn’t go to the doctor. Had a “stressful event” 6 hrs before coming in and felt “weird”. Went to urgent care where an ECG was recorded, and was sent to us for his abnormal ecg.  No prior ekg except for the one done at urgent care. He mentioned he would get brief palpitations once in a while, mostly with heavy exertion, but very infrequently and none for years.”

Here is the ED ECG:

This was the ECG recorded 20 minutes prior in Urgent Care:

First, a comment, then my answer below:

I have noticed that readers of this blog are more interested in reading posts on tachydysrhythmias than in reading posts on OMI.

Why is that?

In my opinion, tachydysrhythmmias are relatively easy for 2 reasons:

1) when there is a tachydysrhythmia, you know you have a problem (tachycardia) and 2) you can get help from cardiologists who are good at this sort of problem.

But when you have a patient with chest discomfort, SOB, jaw pain, epigastric pain, etc.:

1) it is very infrequently due to OMI (about 2-5%, half of which are obvious STEMI). So you don’t know you have a big problem UNLESS you can recognize subtle OMI on the ECG. And 2) Cardiologists are not good at recognizing subtle OMI, so you can’t rely on your help.

And when I post these tachydysrhythmia ECGs, and viewers see them, they immediately see there is a problem and want to know the answer. But when I post a subtle OMI ECG, viewers often see nothing (just like many cardiologists) and so lose interest.

The irony is that those subtle OMI ECGs are the ones that it is most important to learn from!

My answer:

“First, I would look at the heart and see whether there is a good ejection fraction or not. I would also look in the medical record to see if the patient has any chronic left ventricular disease, especially ischemic heart disease, or any kind of cardiomyopathy. If he does, then it is likely standard VT, which responds to procainamide. If he is otherwise healthy, and especially if he is young, then I think about things like right ventricular outflow tract. He is 60’ish years old, so not young!”

“Electricity is always the safest way to convert tachydysrhythmias, but it will not prevent recurrence, so it is not indicated here (see below).”

Remember thought that adenosine is safe for any kind of VT.

I continued: “The ECG has a morphology typical of right ventricular outflow tract VT (RVOT). [RVOT is one of the “idiopathic ventricular tachycardias.”  It is not certain that it is RVOT because it is a bit wider than I would expect, but RVOT responds well to adenosine and adenosine is safe in any kind of VT, so in that case I would start with adenosine. If that did not work, my next step would be procainamide.  The procamio study showed it to be both more effective and safer than amiodarone for standard monomorphic VT.   Beta blockers should work for RVOT, but if it is typical monomorphic VT (not RVOT) due to cardiomyopathy or scar with poor LV function, BB could precipitate cardiogenic shock. 

So I would only give beta blockers if there is very good LV function.”

RVOT morphology (Ken goes into more detail below): the impulse originates from the Right ventricular outflow (just as the name suggests!). In other words, it originates from the superior right side. Therefore, the impulse will travel towards the inferior wall and from right to left. Therefore, it will have an inferior axis and also a left bundle branch block morphology.

RVOT, if continuous, usually responds to adenosine.

I continue: “The problem with adenosine or electricity in this case is that this VT is clearly intermittent.  Look at the urgent Care ECG: there are moments when the VT terminates and there is a least 1 sinus beat. Thus it is recurrent VT.”

Thus, I responded: “You can tell from this EKG that electricity is not going to work, just like adenosine will not work. That is because both therapies are very short in duration, such that the VT might convert, but will return. I know that because of that one pause where there was a sinus beat. The VT terminated for one second, but then it recurred. This tells you that you will definitely need an antidysrhythmic agent.”

Eventually after talking to cards we gave 2.5 of metoprolol, which helped and then another 10 converted him into NSR.

Final Diagnosis was RVOT

Beta blockers are the treatment of choice for RVOT.

Here are more cases of RVOT: RVOT (right ventricular outflow tract ventricular tachycardia)

Here is a very nice summary of RVOT from StanfordHealthCare.

Another well-known idiopathic VT is “Posterior Fascicular VT“, which has an RBBB and LAFB morphology (since it arises from the postrior fascicle) and is responsive to verapamil. Here is another case of idiopathic posterior fascicular VT.

Here is a nice summary of Idiopathic Ventricular Tachycardias for the EM Physician

======================================

MY Comment, by KEN GRAUER, MD (7/5/2025):

One of the most challenging problems faced by emergency care providers regards assessment of the regular WCT (Wide-Complex Tachycardia). Such is the challenge that was presented to Dr. Smith — when he was asked to assess today’s ECG — told only that the patient was a man in his 60s with a history of intermittent palpitations over time, primarily brought on during exertion.

For clarity in Figure-1 — I’ve reproduced this patient’s initial ECG that was recorded on arrival to the ED ( = ECG #1) — as well as this patient’s ECG that was recorded ~20 minutes before ECG #1, when he was seen at the Urgent Care Center ( = ECG #2).

==========================

My Thoughts on ECG #1:

The ECG in Figure-1 is a regular WCT at ~180/minute, without clear sign of atrial activity. As we’ve discussed on frequent Posts in Dr. Smith’s ECG Blog — the principal differential diagnosis is between: i) VT (Ventricular Tachycardia) — vs — ii) An SVT (SupraVentricular Tachycardia) with either preexisting BBB (Bundle Branch Block) or rate-related aberrant conduction.

• We have reviewed ECG assessment of regular WCT rhythms on many occasions (See My Comment at the bottom of the page in the March 6, 2025 post, among many others).
• First, assuming today’s patient is hemodynamically stable (as we may presume he is — given that he was sent to the ED from the Urgent Care Center) — the “good news” is that by definition, there is at least a moment of time to contemplate this patient’s initial ECG (ie, Regardless of the rhythm — immediate cardioversion would have been indicated if the patient was unstable with a regular WCT).
• I favor starting with “statistics” in the stable adult who presents with a regular WCT. Given this patient’s age (in his 60s) — statistical odds that a regular WCT rhythm without P waves will turn out to be VT is at least 80% (and closer to 90% if the patient has underlying heart disease — even before you begin to analyze the ECG).
• As per Dr. Smith — ECG #1 in today’s case manifests a QRS morphology suggestive of OT VT (Outflow Track VT) — because: i) There is an inferior frontal plane axis (ie, lead aVF predominantly positive — compared to lead I being almost isoelectric); and, ii) The QRS morphology in the chest leads resembles LBBB conduction (ie, entirely negative QRS in lead V1 — and all positive QRS in lead V6).
• The reason ECG #1 is almost certain to represent VT (and not LBBB conduction in a patient with SVT) — is that unlike LBBB conduction, in which the QRS remains predominantly negative for most chest leads until leads V5 or V6 — the area of transition in ECG #1 occurs within the BLUE rectangle ( = between leads V2-to-V3), which is far too early to be consistent with supraventricular conduction. Therefore — the rhythm in ECG #1 is all-but-certain to be VT.

Idiopathic VT:

As we’ve periodically reviewed — Idiopathic VT is a special form of ventricular tachycardia, in which the patient does not have underlying structural heart disease (See My Comment — at the bottom of the page in the February 14, 2022 post).

• Depending on the population surveyed — one of the forms of idiopathic VT make up ~10% of all VTs seen in practice. As I summarize below in Figure-2 — the clinical significance of distinguishing idiopathic forms of VT from the much more common ischemic and structural forms of VT — is that evaluation and treatment are very different, with in general a much better longterm outcome and response to treatment with the idiopathic VTs.

==========================

Figure-1: I’ve reproduced the 2 ECGs in today’s case. (To improve visualization — I’ve digitized the original ECGs using PMcardio).

==========================

What about ECG #2?

As per Dr. Smith — ECG #2 (that was done ~20 minutes before ECG #1 — while the patient was at the Urgent Care Center) — provides us with several important insights!

• Runs of VT are interrupted by several sinus-conducted beats (beats #5, 25 and 27). The much narrower and very different QRS morphology for sinus-conducted beats + the post-ectopic pauses after beats #4, 24 and 26 — in association with the constant coupling intervals of the wide beats confirm that the regular WCT rhythm in ECG #1 was indeed VT.
• The intermittent nature of this WCT in ECG #2 convinced Dr. Smith of the need for antiarrhythmic treatment — since the effect of Adenosine wears off in seconds.
• Adenosine is not effective for the vast majority of VT rhythms, which are ischemic or structural in etiology. In contrast (as per Dr. Smith) — the idiopathic VTs (especially the OT VTs) are often adenosine-responsive! As a result — it would have been reasonable after seeing ECG #1, to try Adenosine in the ED, since it often works for the OT VTs. However, once the Urgent Care tracing became available — awareness of the intermittent nature of this patient’s WCT strongly suggests a longer-acting agent (such as the IV Metoprolol that was used) is a much better treatment choice.

Was this RVOT VT – or – LVOT VT?

As emphasized in my summarizing Table in Figure-2 — by far, the most common form of idiopathic VT are the OT VTs. Of these — RVOT VT (Right Ventricular Outflow Track VT) is much more common than LVOT (RVOT making up almost 90% of the OT VTs).

• QRS width with the OT VTs is variable — often depending on whether the location of the OT VT is of septal origin (often with QRS duration <140 msec.) — vs of free wall origin (typically with QRS duration of ≥140 msec.) — Shimizu in Heart Rhythm 6(10): 1507-1511, 2009.
• Whereas RVOT VT is usually not difficult to recognize on ECG (ie, Chest leads showing LBBB conduction with an inferior frontal plane axis). In contrast — LVOT VT is more variable in its ECG presentation. As described in Figure-2 — I thought today’s ECG fit better with the typical description of LVOT VT because transition occurs earlier than is typical for RVOT VT (ie, within the BLUE rectangle in ECG #1).
• The above said — clinical response to treatment of RVOT VT and LVOT VT is similar in an emergency situation.

==========================

Figure-2: Review of KEY features regarding idiopathic VT.

===================================