Very fast narrow complex tachycardia

A 50-something with h/o palpitations, chest pain, and EF of 40% (of unknown etiology) presented with chest pain.

Blood pressure, perfusion, and mental status were normal.  Patient was comfortable appearing.  

Here is his initial ED ECG:

Narrow Complex Tachycardia at a rate of 217

A Modified Valsalva was attempted without success.

Then 6 mg of adenosine was given.  There was a 2 second interruption, and then this rhythm strip was recorded:  

There is now a wide complex, with RBBB pattern.  

For unknown reason, the right bundle no longer repolarizes in time for the next beat.  It is refractory.  So there is now a rate related RBBB even though previously, at the same rate, there was normal conduction.  

RR intervals are ~275 ms, corresponding to heart rate = 218 (= initial heart rate)

Then 12 mg of adenosine was given.

Here is the first half of the rhythm strip after 12 mg:

Here is the second half:

As you can see, there is initial slowing of the ventricular rate and then it speeds up again. 

If you look closely at lead V1, you can see atrial activity throughout, at a very similar rate to the fast ventricular rate.

These are not flutter waves, which would be much large (i.e., "macro"); they are too small.  This is micro-atrial tachycardia. 

Short primer of atrial tachycardia

--Atrial Flutter is a "Macro" tachycardia, with a pathway that uses the entire right atrium and therefore has large, very visible flutter waves.  

--Atrial flutter is also a re-entrant atrial tach.  So it is a "Macro Re-entrant Tachycardia"

--Micro atrial tachycardia takes place in a very localized part of the atrium and manifests on the 12-lead as atrial activity that is of much less magnitude and duration than flutter.

--Micro atrial tachycardia can be either re-entrant or automatic.  

--Automatic tachycardias, including atrial tachycardias, are not responsive to either adenosine or electricity. 

--All re-entrant tachycardias, Macro (flutter) and Micro, are potentially responsive to electrical cardioversion. 

--Of Micro re-entrant atrial tachycardias, some are adenosine responsive and some are not.  

--When you treat an SVT with adenosine and it converts, you can't be certain that it was AVNRT -- it might have been a micro-reentrant atrial tachycardia that is adenosine responsive!

--With any atrial tachycardia, the ventricular rate can be reduced by an AV nodal blocker such as beta blocker or calcium channel blocker.

Back to our case

This atrial tachycardia is not macro; it is micro.  This one does not appear to respond to adenosine.   As soon as the short half-life adenosine is metabolized, the AV node can conduct again and the ventricular rate is fast again.  

But at this very fast atrial rate, the atrial tach is probably re-entrant and it should respond to electricity. 

Many AV nodes cannot conduct this fast and, if they do not, we would see 2:1 conduction with a heart rate of about 109.  This AV node conducts very fast.

Just like with atrial flutter or fibrillation, we can slow the ventricular response with an AV nodal blocker that lasts longer than adenosine, such as a calcium channel blocker or beta blocker.

Of course, we could just try electricity to see if it will convert this atrial tachycardia (it should be successful if it is re-entrant). Electricity is very likely to work.

The patient was a bit reluctant to be electrically cardioverted, so we gave him metoprolol 5 mg IV q 5 minutes x 3 (total dose = 15 mg)

Here is his ECG rhythm strip after metoprolol:

Mostly 2:1 conduction, with some 1:1 conduction.  

Here you can see where I marked the atrial activity in lead V1.  

And a 12-lead:

These show mostly 2:1 conduction, with some beats conducting at 1:1

After this, the patient agreed to electrical cardioversion:

Normal Sinus Rhythm

Why did the patient have a low EF?

--He probably had been having such frequent tachycardia that he had tachycardia cardiomyopathy.

He underwent an angiogram which was normal.

He later reverted to atrial tachycardia while an inpatient.

2 days later, he underwent EP study with ablation.

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MY Comment, by KEN GRAUER, MD (8/23/2022):

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I found today's case fascinating, with a number of important lessons. I fully acknowledge that after pondering the intricacies of the 7 tracings shown above by Dr. Smith — I had more questions than answers. That said, despite a number of uncertainties — the lessons are clear! — and, excellent management by Dr. Smith resulted in successful conversion to sinus rhythm.

• I focus my comment on 4 of the 7 tracings shown by Dr. Smith above. For clarity — I've numbered the tracings in the sequence that were shown above.

The patient in today's case presented with chest pain — and the ECG shown in Figure-1. The patient was hemodynamically stable in association with this rhythm.

• Even before addressing the rhythm — the 1st point to make is that patients with tachyarrhythmias often present with chest discomfort. IF the patient's chest pain promptly resolves on conversion to sinus rhythm and this post-conversion ECG shows no acute ST-T wave changes — then you can usually be comfortable that the chest pain was merely a result of the rapid heart rate, and not an acute cardiac syndrome.

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

MY Thoughts on the Initial ECG:

The ECG in Figure-1 shows a regular narrow-complex tachycardia — therefore, a regular SVT (SupraVentricular Tachycardia). The heart rate is ~215/minute. The presence of atrial activity is uncertain.

• Although there is an upright deflection just past the midpoint of the R-R interval in lead II — the heart rate of ~215/minute is too fast for this to represent a sinus P wave.
• Leads V1 and aVR both manifest what might be a pseudo-r' that notches the terminal portion of the QRS in those leads. Retrograde atrial conduction with AVNRT often looks like this in these 2 leads. That said — when we do see retrograde atrial activity with AVNRT — it typically produces a negative notch in the terminal part of the QRS in the inferior leads, and that is not seen in Figure-1.
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• Bottom Line Regarding Atrial Activity in Figure-1 — I could not be certain as to whether some type of atrial activity was or was not present.

Therefore — My assessment of the ECG in Figure-1 was that there was a regular SVT rhythm at ~215/minute, without clear sign of atrial activity.

• We've previously reviewed the differential diagnosis of regular SVT rhythms on many occasions in Dr. Smith's ECG Blog (Please see discussions by Dr. Smith and My Comment at the bottom of the page of the March 6, 2020 post for Review of Key Concepts).
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• Practically Speaking — the principal differential diagnosis of a Regular SVT rhythm, in which sinus P waves (ie, a definite upright P wave in lead II) are not evident includes: i) Sinus Tachycardia (IF there is a possibility that sinus P waves might be hiding within the preceding ST-T wave); ii) A Reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an AP [Accessory Pathway] located outside the AV node is involved); iii) Atrial Tachycardia; or iv) Atrial Flutter with 2:1 AV conduction.
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• Heart Rate Can Help! In brief — i) IF the heart rate in an adult is ≥170/minute — then both Sinus Tachycardia and AFlutter become less likely (ie, not impossible! — but less likely); — BUT — ii) IF the heart rate of a regular SVT rhythm in an adult is close to ~150/minute (ie, ~140-160/minute) — then any of the above 4 entities have to be considered in the differential diagnosis!

Applying this to the rhythm in Figure-1:

• As noted above — the heart rate of ~215/minute in ECG #1 makes sinus tachycardia in an adult extremely unlikely.
• Untreated AFlutter is also extremely unlikely — since a rate of ~215/minute is too fast for 2:1 AV conduction (because this would require a flutter rate of 215 X 2 = 430/minute — which is much faster than the usual flutter rate of ~300/minute) — and a rate of ~215/minute is slower that what one would expect if there was 1:1 conduction with AFlutter.
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• This leaves a reentry SVT or ATach as the most likely possibilities for the rhythm in Figure-1.

The "Good News" about Treatment:

• While helpful to work through the differential diagnosis — initial management of regular non-sinus SVT rhythms in an ED setting is very similar.
• During the course of such treatment — you will usually arrive at the correct rhythm diagnosis.

The CASE Continues:

In today's case — Valsalva was unsuccessful. Adenosine was then given (initially 6 mig IV — then 12 mg IV). The result is seen in the 2 rhythms shown in Figure-2.

• NOTE: To facilitate visualization of key features — I only show leads V1,V2,V3 for the 2 rhythms in Figure-2.

Figure-2: ECG #3 — and its continuation in ECG #4 illustrate the response of the regular SVT rhythm to Adenosine (See text).

The Response to Adenosine:

Having all but eliminated sinus tachycardia and atrial flutter (because of the very rapid rate of ~215/minute) — the differential diagnosis for today's regular SVT rhythm was reduced to some form of reentry SVT (ie, AVNRT or orthodromic AVRT) or ATach.

• Adenosine will almost always work for converting a reentry SVT rhythm. 
• As per Dr. Smith's discussion above — Adenosine may or may not convert ATach, depending on the mechanism of the ATach.
• Most of the time, even if Adenosine does not convert the rhythm — this drug's effect on slowing the ventricular response to the SVT (at least, for the brief duration of action of Adenosine) — will allow underlying atrial activity to be seen, thereby revealing the mechanism of the rhythm. 

The unique feature of today's case is that shortly after Adenosine was given — RBBB conduction developed! (seen for beats #1-20 in ECG #3).

• Failure of 2 doses of Adenosine to convert the regular SVT rhythm in today's case suggested that the etiology was likely to be ATach.
• My understanding from review of the literature is that induction by Adenosine of RBBB during treatment is rare (because Adenosine generally has little or no effect on conduction through ventricular myocardium or in the bundle branch system).
• The typical rsR' morphology in lead V1 for beats #1-thru-20 in ECG #3 and the fact that the rate of the rhythm during these 20 beats was identical to the ~215/minute seen in Figure-1 — strongly suggested that this was indeed induction of a supraventricular RBBB conduction pattern by Adenosine (and not VT).
• Although a component of "rate-related" BBB appeared to be operative — the fact that the heart rate before and after onset of RBBB conduction remained the same suggested some other mechanism accountable for the switch to RBBB conduction. Perhaps in today's patient Adenosine did exert some effect on conducting tissues within the bundle branch system that took effect before the drug was able to act on AV nodal tissue?
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• Beat #21 in ECG #3 is conducted normally. Perhaps the short pause before this beat was enough to normalize bundle branch conduction?
• Beats #23 and 26 look like PVCs (very different morphology). But what about beats #22, 24,25,27,28,29?

Take a look at ECG #4. Note that there are 3 different QRS morphologies seen on this rhythm strip!

• The challenge interpreting ECGs #3 and #4 — is that we only intermittently see atrial activity (and we really only see atrial activity in lead V1).
• I suspect Dr. Smith is correct that atrial activity continues throughout both rhythm strips — but we really are not able to consistently follow such atrial activity (ie, RED arrows show those regular P waves that we can see in the 2nd half of ECG #3 — and in the 1st half of ECG #4 — but there really is no "telltale notching" under the PINK arrows — so can we really be certain that atrial activity stays regular throughout these tracings?).
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• BLUE arrows in ECG #4 suggest continuation of regular atrial activity — BUT — note that while the PR interval for RED arrow P waves appears to be constant — this PR interval is different than the PR interval of every-other-BLUE-arrow P wave that appears to be conducting.
• Finally — the YELLOW arrow P wave appears to conduct — and sets up return of 1:1 conduction with the same RBBB morphology that was seen at the beginning of ECG #3.

BOTTOM LINE: Other than the 2 PVCs (ie, beats #23 and 26 in ECG #3) — I suspect all beats in Figure-2 are supraventricular. ECG #3 begins with the RBBB conduction induced by Adenosine — until finally, Adenosine's effect begins to act on the AV node with beat #22.

• Perhaps the unusual action of Adenosine in today's patient — that is acting on both bundle branch tissue and AV nodal tissue — accounts for the 3:1 AV block with a different (wider) QRS morphology at the end of ECG #3 and the beginning of ECG #4?
• There then follows normal QRS conduction with 2:1 block during the period of BLUE arrow P waves.
• ECG #4 then finishes with the YELLOW P wave that initiates 1:1 conduction with the original RBBB morphology for beats #12-thru-23 in ECG #4.

Metoprolol was then added (3 doses of 5 mg IV over 10 minutes) — and ECG #6 was recorded (Figure-3):

Figure-3: ECG #6 was obtained followed 3 doses of IV Metoprolol.

The Response to IV Metoprolol:

Note in ECG #6 that atrial activity is only seen in lead V1 (colored arrows in this lead). It would be easy to overlook the presence of P waves if you did not carefully scrutinize lead V1!

• Note that the overall ventricular rate has slowed. In addition — the effect of Adenosine has worn off by this time. As a result — the QRS complex is narrow!
• We have deduced that the rhythm in today's case is ATach.
• Note that there is group beating in parts of the long lead II rhythm strip in Figure-3 (ie, a number of bigeminal beats spread out over the long lead rhythm strip).
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• PEARL #1: ATach frequently manifests Wenckebach conduction. Because we don't see atrial activity in lead II — the long lead rhythm strip is of little use to us in assessing the mechanism of this rhythm. But the 5 beats we do see in lead V1 are revealing — as there is 3:2 Wenckebach conduction (Each cycle begins with the shortest PR interval [RED arrows] — followed by lengthening of the PR interval [BLUE arrows] — and then the dropped beat [WHITE arrows] to complete the Wenckebach cycle).
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• PEARL #2: A characteristic of ATach — is that P wave morphology of the atrial focus is often quite different from the morphology of sinus P waves. Note in the last tracing shown above (after electrical cardioversion) — that a normal upright sinus P wave is now seen in lead II.

KEY Lessons to Be Learned:

The management course outlined above by Dr. Smith was appropriate and effective! As per Dr. Smith — Adenosine is often the optimal choice in the ED for initial management of the regular SVT rhythm.

• Adenosine effectively slowed the rhythm in today's case — thereby allowing identification of the correct etiology ( = ATach).
• That said — Adenosine did not convert the rhythm to sinus.
• It appears that Adenosine produced the unusual effect of inducing RBBB conduction (at the identical rate as the initial narrow SVT rhythm). Awareness that this side effect can be seen with Adenosine is important — as is recognition that persistence of the identical 215/minute heart rate essentially ruled out VT as the cause for QRS widening.
• Along the way (during the 1-2 minutes that IV Adenosine was active) — a variety of unusual arrhythmias (with different QRS morphologies and changing PR intervals) were seen. As fascinating as this mixture of arrhythmias was — there is no need for in-depth arrhythmia analysis during the time that Adenosine is active because: i) Adenosine-induced arrhythmias are often complex and "don't read the textbook"; and, ii) Adenosine-induced arrhythmias almost always resolve when the drug wears off.
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• When the SVT rhythm persisted in today's case despite Adenosine administration — We can take comfort knowing that another antiarrhythmic and/or electrical cardioversion will almost always work.