Wide Complex Tachycardia -- VT, SVT, or A Fib with RVR? If SVT, is it AVNRT or AVRT?

A 69 y.o. male with pertinent past medical history including Atrial fibrillation, atrial flutter, cardiomyopathy, Pulmonary Embolism, and hypertension presented to the Emergency Department via ambulance for respiratory distress and tachycardia. 

Per EMS report, patient believes he has been in atrial fibrillation for 5 days, since coming down with flu-like illness with rhinorrhea, productive cough, SOB. Patient is on rivaroxaben, carvedilol, and dofetilide (to suppress atrial fib -- rhythm control).  He states that he maybe missed a dose or two during recent illness. On EMS arrival, patient's oxygen saturation was in the high 80s and improved on 4L O2 via nasal cannula. 

He was noted to have irregular heart rhythm with rates 120-170s. BG 248. 

Bedside ultrasound showed volume depletion and no pulmonary edema.

Here is the prehospital ECG:

First ED ECG

What do you think?

Description: Regular Wide Complex Tachycardia at a rate of about 160.  VT?  SVT with aberrancy?  If SVT, is it AVRT or AVNRT?  It appears too regular to be atrial fib with RVR

I inspected this carefully and it is very regular.  Thus, it really cannot be atrial fibrillation

Is it Ventricular Tachycardia, which is usually a regular rhythm?

Smith opinion: I at first thought this was VT and would have electrically cardioverted.  But I changed my mind after seeing the old ECG (below)

I later sent it to Ken Grauer, who annotated as below with the red Xs:

The "Y" in lead II across the bottom appears to be a PVC.  

Thus is it almost impossible that this is VT, even without the old ECG.  Since it is regular, it must be PSVT (AVNRT or AVRT).    

Thus, adenosine is very likely to work here.

 

______________________

If you want to know more detail (skip if you do not need so much detail), especially if it is AVNRT or AVRT, Ken writes the below, where he also agrees that it cannot be atrial fibrillation:

There are 2 places with this otherwise very regular WCT is “interrupted”. The 1st place ( = X) is kind of bizarre, in that QRS morphology look very similar in leads I,II,III — but a little earlier and narrower (almost like this beat may have occurred during the “supernormal conduction” period ( = a truly RARE phenomenon).

But the 2nd interruption = Y — looks to be a PVC — which is why, even before seeing the prior tracing, I suspected this initial ECG was supraventricular (and not VT).  

Smith: this is because it is almost impossible to have a PVC in the midst of VT

I measured intervals with calipers on my big screen — and other than these 2 interruptions, find the rhythm VERY regular. I don’t see evidence of retrograde atrial activity during the WCT — but usually with the “almost regular AFib rhythms” — you can when you measure pick up some slight differences — so my hunch is that the initial ECG is a REENTRY SVT rhythm, that then breaks down to AFib.

Now you CAN on occasion see PVCs during reentry SVTs that do not convert the SVT. Theoretically  — this can occur with BOTH AVNRT and AVRT. In theory, a PVC is more likely to convert AVRT — because part of the reentry pathway is OUTSIDE of the AV Node (ie, passing thru the AP) — and therefore a PVC would be more likely to “run into” the reentry pathway, and convert the rhythm.

In theory, with AVNRT — the reentry pathway is completely contained WITHIN the AV node — so a PVC would seem LESS likely to convert AVNRT, because it “can’t get to” the reentry pathway that is entirely within the AV node — so my hunch is this initial ECG was AVNRT ________________________

The patient was stable enough to look for a previous ECG.  Here it is:

Slow atrial fibrillation, rate controlled with carvedilol presumably

This shows the same QRS morphology (RBBB + LPFB), proving that the rhythm above is supraventricular, and NOT VT (as suspected by the PVC)

The providers realized it was not VT, but did not recognized it as SVT with RBBB/LPFB.  Instead they diagnosed it as Atrial Fib with RVR.

Thus, they did not give adenosine.

A patient who has atrial fib and is on dofetilde is on a "rhythm control" strategy for AF.  Dofetilide is used for atrial fib rhythm control, not for rate control.

The appropriate management would be to give IV fluids first to restore volume in this patient whom they believed had pneumonia as the initiating factor.  I'm not sure if they started with this, but let's assume that they did.

If you think this is atrial fibrillation with RVR, then because the patient is anticoagularted, one could safely sedate and cardiovert.  Of course, this is NOT atrial fib, but rather PSVT, and so adenosine should work. (Some are now advocating for calcium channel blockers, but that discussion is for another day).

The patient did not want to be electrically cardioverted, so they gave metoprolol.

t = 14 minutes, after giving IV metoprolol

Now there is atrial fibrillation with a much slower rate and PVCs.

Metoprolol can sometimes convert SVT, and sometimes the rhythm can change to atrial fibrillation.

t = 16 minutes

Further Care in the ED:

1. Patient hemodynamically stable, discussed options with patient, would prefer medications before attempting cardioversion
2. Patient given metoprolol 5 mg IV with improvement in HR to 110-120s, repeated ~q5 mins x3. Patient also given metoprolol PO 50 mg. 
3. Mag 2g administered 
4. Appeared mildly hypovolemic on US, LV function grossly preserved, reports decreased PO intake, given gentle 500 cc bolus
5. CXR with likely infiltrates vs edema, blood cultures collected, started ceftriaxone and azithromycin
6. Given patient reports not having taken home meds today, given home dofetilide, coreg and xarelto
7. Labs notable for mild Acute Kidney Injury (Cr 1.5). pH 7.4. 
8. CT noncon prelim consistent with pneumonia, final read pending
9. Patient's HR 110s, respiratory effort improved, reported symptomatic improvement

Later in afternoon

After a brief hospital stay, the patient was discharge, still in atrial fibrillation.

On a visit 2 months later, he was cardioverted.

Back to basics: what is this rhythm? What are your options for treating this patient?

Written by Bobby Nicholson MD, with edits by Meyers, Smith, Grauer

A woman in her early 40s presented to the emergency department for evaluation of palpitations.  She reported that she has been experiencing this since she was diagnosed with COVID a little over 1 week ago. She reported a prior history of SVT and has previously performed vagal maneuvers at home with symptom resolution.  She reports that she is now unable to vagal out of her palpitations and is having shortness of breath and dull chest pain. Her initial EKG is below.

We see a regular tachycardia with a narrow QRS complex and no evidence of OMI or subendocardial ischemia. The differential of a regular narrow QRS tachycardia is sinus tachycardia, SVT, and atrial flutter with regular conduction. There are no P waves preceding the QRS complexes, and no clear flutter waves. SVT is by far the most likely rhythm in this case. 

There are retrograde P waves seen immediately after the QRS complex in most leads. They are inverted in lead II, for example.

She was treated with 6mg adenosine rapid IV push. The following EKG was obtained after administration of adenosine.

Now the patient is in sinus tachycardia. Unfortunately, shortly after this EKG was obtained, the patient returned to SVT.

 

Same as initial ECG.

Smith: should we give adenosine again?

Smith: No!  Adenosine worked.  It converted the rhythm.  But adenosine only lasts for seconds, and if the dysrhythmia recurs, then the adenosine is gone.

We need to do one or both of two things:

1. Prevent the initiation of the dysrhythmia -- this can be done with a beta blocker by prenenting PACS

2. Have a long acting AV nodal blocker -- this can be done with a longer acting AV nodal blocker: both a beta blocker or calcium channel blocker.  

Metoprolol  (beta blocker) thus does BOTH

1. Prevents the PAC that initiates SVT
2. Blocks the AV node to prevent propagation.

Diltiazem and Verapamil (Calcium channel blockers) block AV conduction        

Dosing

• Metoprolol
• 5 mg IV q 5 minutes x 3 (max 15 mg), then 25-50 mg orally.
• Verapamil
  • Dosed at 2.5-5 mg IV over 2 min (over 3 min in elderly patients).
  • A follow-up dose of 5-10 mg (0.15 mg/kg) IV is administered 15-30 min later if the SVT persists and no adverse reaction occurs. The maximum dose is 20-30 mg.
  • This may be followed by an infusion of 0.005 mg/kg/min.
• Diltiazem
  • Dosed at 0.25 mg/kg IV over 2 min.
  • A subsequent dose of 0.35 mg/kg IV is administered if no response is seen and no significant drug-induced adverse event occurs

She remained hemodynamically stable and was treated with 10 mg of IV diltiazem. The following EKG was obtained

 

After treatment with diltiazem, the patient remained in normal sinus rhythm with a rate persistently in the 80s and 90s.

Given recurring SVT without obvious resolution of its cause, she was admitted for further observation and did not have any recurrence. She had an echocardiogram which was normal. She was prescribed oral diltiazem to prevent recurrence and was discharged.

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

MY Comment, by KEN GRAUER, MD (10/25/2022):

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

Today’s blog post reviews the important topic of how to approach the patient who presents with palpitations from an SVT (SupraVentricular Tachycardia) rhythm. I focus my comments on a number of additional points aimed at supplementing the above excellent discussion by Drs. Nicholson and Meyers.

• Today’s patient is a 43-year old woman with a history of intermittent “SVT” that in the past has responded to vagal maneuvers that she performed on herself at home.

Some General Thoughts on SVTs:

I’ve previously reviewed in detail an approach to the regular SVT (Please see My Comment — at the bottom of the page in the March 6, 2020 post in Dr. Smith’s ECG Blog). Relevant points from that discussion that relate to today’s case include the following:

• Knowing that today’s patient had a history of intermittent “SVT” does not tell us the specific rhythm involved. Even experienced providers make the mistake of using the term, “SVT” as a specific diagnosis — when in fact this generic term includes all arrhythmias in which the rate is “tachycardic” (ie, ≥100 in an adult). This includes sinus tachycardia, atrial fibrillation or flutter, MAT, and others. Causes and treatments for these various forms of “SVT” may differ.
• The above said — the fact that today’s patient describes success with home vagal maneuvers strongly suggests that we are dealing with some type of reentry SVT rhythm.
• 
  
• For optimal initial and longterm care of today’s patient — additional features in the History to inquire about include the following: i) How long this patient has had SVT? — How often she gets it? — and — How long it takes vagal maneuvers to work?; ii) Are there any specific precipitating factors? (ie, dehydration, periods of increased stress or anxiety, stimulants such as caffeine, alcohol, recreational drugs, etc.); iii) How often has she had to go to the ED for her SVT?; and, iv) Previous treatments tried?

Diagnosis of Today’s Rhythm:

I favor a systematic approach to rhythm interpretation — in which the memory aid, “Watch your Ps, Qs and 3Rs” reminds me of the 5 KEY parameters to assess (CLICK HERE — if interested in more on this Ps, Qs, 3R approach).

• For clarity in Figure-1 — I’ve reproduced and labeled the initial ECG in today’s case, with the follow-up 12-lead after administration of 6 mg IV Adenosine.
• 
  
• Applying the Ps, Qs, 3R Approach to ECG #1 — there is a regular SVT ( = narrow QRS) rhythm at a rate of ~140/minute, without sign of sinus P waves. 
• 
  
• PEARL: It’s important to keep in mind the importance of the rate of a regular SVT rhythm — since since entities such as sinus tachycardia (with sinus P waves hidden within preceding T waves) and atrial flutter (with 2:1 AV conduction) become become far less likely when the rate of a regular SVT exceeds ~170/minute. 
• In contrast, a regular SVT rhythm at a rate between ~130-160/minute (as in today’s case) — includes a differential diagnosis of i) Sinus tachycardia; ii) AFlutter (Atrial Flutter); iii) ATach (Atrial Tachycardia); and/or, iv) A “reentry” SVT rhythm (with AVNRT and orthodromic AVRT being the most common forms of this).

CHALLENGE:

Compare QRS morphology for the 2 ECGs shown in Figure-1. With attention to the RED arrows in ECG #1 — What is the difference in QRS morphology between these 2 tracings?

• Clinically — What is the significance of this difference?

Figure-1: The first 2 ECGs in today’s case. What is the clinical significance of the RED arrows in ECG #1?

Those RED Arrows in ECG #1:

The RED arrows in Figure-1 highlight 7 leads in ECG #1 that show retrograde atrial activity during the tachycardia.

• PEARL: The clinical significance of identifying retrograde atrial conduction during a regular SVT rhythm (such as the one in today’s case) — is that it confirms the diagnosis of a reentry SVT rhythm! Sinus tachycardia, AFlutter and ATach do not do this. 
• To Emphasize — It is not common to see clear evidence of retrograde conduction in as many leads as shown by the RED arrows in ECG #1. The reason I highlight this finding — is that knowing how to look for retrograde atrial activity is helpful when its presence is far more subtle. This is because once we can confirm the diagnosis of a reentry SVT — we know what optimal treatment in the ED will be if our initial dose of Adenosine is ineffective (ie, repeat Adenosine and/or Diltiazem, Verapamil or a ß-Blocker).

How to Confirm Retrograde Conduction:

Retrograde conduction produces a negative P wave that appears after the QRS in the inferior leads. This is because the retrograde impulse is traveling away from the direction of lead II, which is positively oriented at +60 degrees.

• As a result, when looking for retrograde atrial activity — I first focus my attention on the very last part of the QRS in the inferior leads (II,III,aVF) — looking for a negative notch or deflection in one or more of these leads. The wide, “pseudo-S wave” seen in each of the inferior leads in ECG #1 is distinctly unusual, especially given the absence of RBBB conduction. Proof that this truly represents retrograde atrial conduction in ECG #1 — is forthcoming by comparison of these leads in ECG #2, in which this negative “pseudo-S wave” deflection in the inferior leads after conversion to sinus rhythm is much narrower.
• 
  
• After the inferior leads — I look next at right-sided leads aVR and V1 — which commonly show retrograde conduction as a short positive “pseudo-r’ deflection” (RED arrows in leads aVR and V1 in ECG #1). Note that this pseudo-r’ deflection is no longer present in ECG #2 after conversion to sinus rhythm.
• Sometimes lead aVL shows retrograde conduction as a positive deflection after the QRS (as seen in ECG #1). 
• In my experience — it is less common to see retrograde conduction in other leads.
• 
  
• HINT: The way to get good at recognizing retrograde conduction during regular SVT rhythms — is to routinely go back and compare deflections that you thought looked suspicious during the tachycardia — with QRS morphology in those same leads after conversion to sinus rhythm. BOTTOM Line: It’s nice to be able to definitively diagnose that the cause of the regular SVT rhythm in front of you is a reentry SVT. Identifying retrograde atrial conduction during a regular SVT rhythm allows you to do so.
• CAVEAT: The opposite is not necessarily true — because some cases of AVNRT manifest such a short RP’ interval, that the retrograde P wave is hidden within the terminal part of the QRS (and therefore not visible on ECG).

PEARL: The RP’ interval (ie, distance of the retrograde P wave from the preceding R wave) — can provide a clue to the mechanism of the reentry SVT. For example — very short RP’ intervals (in which the retrograde P wave notches the terminal portion of the QRS complex) — suggest that the reentry circuit is contained within the AV node. In contrast — longer RP’ intervals (in which the retrograde P wave notches a portion of the ST segment) suggest that an AP (Accessory Pathway) which is located “further away” (ie, outside of the AV node) may be participating in the reentry circuit.

• The RED arrows in today’s case suggest a fairly short RP’ interval — that is more consistent with AVNRT.
• For more on the concept of retrograde conduction during a regular SVT rhythm — Please see My Comment at the bottom of the page in the March 6, 2020 post of Dr. Smith’s ECG Blog.

Some Final Thoughts on Today’s Case:

It is not at all surprising that the reentry SVT rhythm in today’s case recurred shortly after IV Adenosine (ie, the half-life of IV Adenosine is less than 10 seconds!). As a result — it should be expected that a longer-acting agent may need to be added to maintain sinus rhythm (as was done with Diltiazem in today’s case). Among considerations that arise following hospital discharge of today’s patient are the following:

• Awareness that in a younger adult without underlying heart disease (ie, unremarkable Echo) — a reentry SVT is a non-life-threatening and usually fairly benign rhythm disturbance. As a result — the main indication for treatment is to control symptoms. How best to do this depends on answers to the series of questions in the History that I suggested above (under Some General Thoughts on SVTs).
• There is no need to immediately refer today’s patient to EP for ablation. Although treatment of reentry SVTs by ablation is highly effective, with an excellent safety record when done in a center with quality results — there remains potential for a small-but-real incidence of complications with this procedure. Patients should be offered a choice for a trial of medication vs ablation for this non-life-threatening arrhythmia. Clearly, EP ablation becomes indicated in patients with frequent refractory SVT recurrences — but not necessarily before.
• The “best” treatment of recurrent reentry SVT is to find and fix a precipitating cause, when one is present. I’ve had pregnant patients who only got their reentry SVTs during their pregnancy. I’ve had other patients who would have frequent SVT recurrences during periods of intense stress/anxiety — with their reentry SVT episodes controlled when these precipitants were controlled. Excess caffeine or OTC sympathomimetics are other potential precipitants that may be easily controlled once identified.
• Commonly used medications to suppress recurrent reentry SVT episodes include Diltiazem, Verapamil or a ß-Blocker. These medications do not necessarily need to be used continually on an indefinite basis. Life circumstances change. My patient with stress-induced SVT did well for months at a time when her stress was controlled. She stopped her daily Diltiazem during lower-stress periods — and then resumed daily Diltiazem when life stressors resurged.
• For patients with infrequent recurrences that are easily controlled with AV nodal blocking agents — use of “prn medication” (ie, with permission for home use by the patient of a dose of Diltiazem, Verapamil, or a ß-Blocker) at the time of a recurrence, and then going into a quiet room — may resolve the SVT within 30-120 minutes, thereby avoiding an ED visit.
• 
  
• BOTTOM Line: Longterm management of the patient with a reentry SVT should be individualized for the life circumstances of the patient at hand. 

A woman in her 60s with palpitations, chest discomfort, and multiple misdiagnoses by both EM and Cardiology!!

 Written by Pendell Meyers

A woman in her 60s was shopping when she suddenly experienced palpitations and chest "discomfort." She denied outright chest pain or dyspnea. She walked across to the street to my Emergency Department. She had no known prior history of dysrhythmias or heart disease, but had known hypertension, breast cancer, diabetes, and obesity. She has had episodes of palpitations in the past, followed by holter monitor workups which did not reveal any cause of palpitations. However, her symptoms today feel worse than prior episodes, and she has never felt the "chest discomfort" with prior palpitations. Upon pointed questioning, she told the providers she has had several similar episodes over the past few weeks, but did not seek care during those episodes and they were shorter.

Here is her triage ECG during active persistent symptoms:

What do you think?

We see a regular, narrow, monomorphic tachycardia, for which the full differential would include sinus tachycardia, SVT (an umbrella term including many different rhythms), and atrial flutter. 

This ECG has a large negative atrial wave just before the QRS complexes in the inferior leads, with only one of these waves visible for each QRS complex. These waves are of course fully upright in V1. The differential includes a low ectopic atrial tachycardia near the AV node, or a relatively high AVNRT such that the circuit activates the atrial retrogradely before the circuit can activate the ventricles anterogradely during each lap of the circuit.

It is not atrial flutter, because with such a prominent atrial wave seen in the inferior leads we should be able to see a second set of these waves midway between the visible ones.

Whatever the atrial waves are, their QRS complexes in the inferior leads are followed by ST segments which seem to be slightly above the baseline in III and aVF. Because I have been fooled by this phenomenon before, and because it does not match OMI patterns I've seen before, I can see that this morphology is likely due to the upright atrial repolarization wave from the dysrhythmia. If there were any question whether it were due to OMI, I would first convert the patient out of this dysrhythmia then reevaluate the ECG for OMI.

The Emergency Medicine team perceived inferior STE in II, III, and aVF, with slight reciprocal STD in aVL, and decided to activate the cath lab for chest discomfort and possible STEMI. Cardiology came immediately and deactivated the cath lab after looking at this ECG and believing that it represented atrial flutter with 2:1 block (this is almost certainly not atrial flutter). 

Approximately 20 minutes later it spontaneously converted to sinus rhythm:

2 hours later it recurred:

She was given 10 mg of diltiazem IV and had conversion back to sinus soon afterward.

Prior ECG on file:

Two high sensitivity troponin I measurements were less than 6 ng/L.

The cardiology team incorrectly diagnosed this rhythm as atrial flutter with 2:1 block.

She was admitted for rate control and "new onset atrial flutter workup."

Echo was normal.

Unfortunately, in the mindset of atrial flutter, the patients CHADS2VASc score was calculated at 3, and she was deemed to require anticoagulation with eliquis (apixaban), which she has been on ever since (several months at this point). I am trying to contact her providers to discuss this.

She was also placed on metoprolol, presumably for rate control during her perceived atrial flutter episodes. In reality, it may be suppressing her SVT (whether it is ectopic atrial tachycardia or AVNRT).

Check out these posts showing atrial repolarization (Ta wave) and how it can cause inferior pseudoSTEMI/OMI patterns:

A man in his sixties with chest pain

Look at this ST Depression (It's not real)

Atrial Repolarization Wave Mimicking ST Depression

K. Wang Video lecture: the Atrial Repolarization Wave (Ta Wave)

Atrial Repolarization wave mimicking ST Elevation:

Sudden CP and SOB with Inferior ST Elevation and in STE in V1. Is it inferior and RV OMI?

A man in his sixties with chest pain

Learning Points: 

Atrial repolarization can be especially visible in ectopic atrial tachycardias (or any dysrhythmia with pronounced ectopic atrial waves), causing the appearance of inferior STE that has nothing to do with OMI.

Diltiazem should not generally cause conversion of atrial flutter to sinus rhythm. Diltiazem converting the rhythm would be more consistent with a reentrant dysrhythmia involving the AV node, such as AVNRT. There is always a chance that the conversion was actually just spontaneous and not associated with the diltiazem.

Misdiagnosis of atrial flutter can lead to significant long term patient harm, especially when treated with anticoagulation. Sometimes getting the rhythm correct is very important. 

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

A young woman in her third trimester of pregnancy had complained of panic attacks on multiple occasions.  

She presented to the ED this time, instead of to a clinic, for the same complaint and her pulse was palpated at "very fast".

Side note: Many panic attacks are diagnosed as SVT by 3 year followup. In other words, the patient was wrongly diagnosed and treated for psychiatric disease for up to 3 years.

Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder. Arch Intern Med. 1997;157(5):537-543. More Info

EMA July 1997: Unrecognized Paroxysmal Supraventricular Tachycardia: Potential For Misdiagnosis As Panic Disorder. EM:RAP. https://www.emrap.org/episode/ema-1997-7/abstract5. Updated September 20, 2017. Accessed September 24, 2020.

Here is the 12-lead ECG:

Narrow complex tachycardia at a rate of 229

She was brought to the critical care area and put on monitors.  Her heart rate on the cardiac monitor constantly changed from narrow complex at 170 to narrow at 230 and back again.

She was hooked up to a continuous 12-lead ECG machine so that the different rates could be recorded.

Here is the slower rate:

Narrow complex tachycardia at a rate of 169

Here I point out the retrograde P-waves with arrows.

So this is clearly a re-entrant paroxysmal SVT (SVT, or PSVT).  But it is at 2 different rates.  Why?

Time zero Trop < 4 ng/L

2 hour = 12 ng/L

No 4 hour troponin was measured, but I suspect it would have been above the 16 ng/L cutoff for acute myocardial injury (for women; 34 ng/L for men), and then she would have been diagnosed with a type II MI.

Type II MI: acute myocardial injury (rise and/or fall of troponin with at least one value above the 99th %-ile upper reference limit AND the injury is due to ischemia AND there is some identifiable source of supply demand mismatch, such as hypotension, anemia, severe hypertension, sustained tachydysrhythmia, etc.)

So this elevated heart rate did cause enough ischemia to result in troponin release.

Here is the post conversion EKG:

Sinus rhythm.  There are no delta waves.  

Absence of delta waves does NOT rule out an accessory pathway.  Some accessory pathways have "concealed conduction," in which delta waves are not evident on the baseline 12-lead because the pathway only conducts in the retrograde direction.

Side note: I was educated today by our electrophysiologist that a syndrome that occurs due to an accessory pathway should only be called WPW if there is a delta wave on the baseline ECG.  So although this patient can have the same orthodromic tachycardias of a patient with WPW, strictly speaking, she does not have WPW.  

This would seem to imply that a patient without a delta wave could not have an antidromic tachycardia (antidromic AVRT) since the accessory pathway cannot conduct in the anterograde direction.  However, some patients can have intermittent WPW; if this were the case for this patient, then she COULD have an antidromic AVRT.  

There is also what is called "latent WPW."  In this case, the transit time from the sinus node through the AV node is faster than the time to get to the accessory pathway, get through it, and begin to Pre-excite the ventricles.

Here is nice explanation of accessory pathways (AP) from Medscape

"An AP that does not manifest on ECG is revealed when the rate exceeds the refractory period of the AV node. This has been described as a latent AP. A latent AP can conduct both antegrade and retrograde transmissions."

"An AP in which only retrograde transmission of impulses can occur is called a concealed AP and is used only during circus movement tachycardia (CMT or ORT). A concealed AP is not detectable on the regular surface ECG findings, because the ventricle is not preexcited. Tachycardia due to a concealed AP should be considered when the QRS complex is normal and the retrograde P wave occurs well after completion of the QRS complex, out in the ST segment or even in the T wave (long R-P tachycardia)." 

Here is an important example of Latent WPW that resulted in failure to diagnose for years.

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

Outcome:

Formal Echocardiogram:

Regional wall motion abnormality-inferior septum/inferior wall.  This strongly supports acute type II MI.

Plan:

She will undergo EP study after delivery.  She was placed on metoprolol until then.

Why were there two different rates?

Usually this is due to simultaneous:

1. "dual AV nodal pathways", which is the source of most SVT (AV nodal reentry tachycardia, or AVNRT) 

2. WITH ADDITIONAL Accessory pathway.

See images far below for dual AV nodal pathways

Most likely Explanation: There are 2 pathways in the AV node, just as there are in all cases of AVNRT.  But in this case, there is a third pathway, probably an accessory pathway.  The reentrant rhythm goes down through the AV node taking one or the other of the 2 pathways, switching back and forth, and up the accessory pathway.  This is an orthodromic SVT, but because the 2 pathways have different conduction velocities, there are 2 different rates.

Provisional Diagnosis: probable Dual AV nodal pathways PLUS bypass tract, with orthodromic SVT that changes rates depending on the AV nodal pathway taken (see images below).  Needs verification by EP study.

This case was kindly reviewed by Dr. Rehan Karim, one of our fine electrophysiologists.  He made the following comment (in addition to informing me that the term WPW is reserved only for those with delta waves):

"There are some other nuances, which might be out of scope of the blog:"

-         "Patients can have “more than one” slow pathways – that could result in multiple cycle lengths of AVNRT’s."

-         "I have had two patients with alternating cycle lengths during same tachycardia (every other beat alternating cycle length, rather than two different tachycardias) – one was accessory pathway mediated (AVRT) retrograde, and antegrade using fast and slow pathways as you have described; another one where patient had AVNRT with two different cycle lengths."

"Therefore, it’s difficult to be certain about it just looking at 12-lead ECG’s – but if I were to guess, the explanation that you give in your description is most likely correct!"

See these two cases: 

Case 1: Wide Complex Tachycardia in a 20 something.

This patient developed ventricular fibrillation from Cardioversion.

Case 2: A Very Fast Regular Narrow Complex, Followed by an Equally Fast Regular Wide Complex

1. Accelerated AV conduction
2. Left lateral accessary pathway

Above: Duel AV nodal pathways.  They have different conduction velocities.  They also have different refractory periods.  This is the substrate of AVNRT.

Dual AV nodal pathways with ADDITIONAL accessory pathway. 

But this circuit is the opposite direction of our patient today!

 

In this schematic, the conduction is ANTIDROMIC (down the bypass tract and up the AV node).  This would create a wide complex tachycardia that may mimic a very fast VT but at 2 different rates, depending on which pathway within the AV node is taken.  See this case.  This would be AV Reciprocating Tachycardia (AVRT).

In our patient, it is ORTHODROMIC: the impulse goes from the atrium to the AV node, then through either the fast or slow pathway (which determines the rate), then back up through the accessory pathway.

A very fast wide complex tachycardia

A 60-something patient presented by EMS with non-specific symptoms.  He had a very rapid rhythm that was not converted by 6 mg, then 12 mg of adenosine.

On arrival, his BP was 94/75, pulse 127.

A bedside cardiac ultrasound was reported as showing good function, but I just viewed it and there is decreased function.

Here is his 12-lead:

Wide complex, Rate 265
("Pulse" was 127, so many of these beats are not resulting in a strong enough pulse to be palpated.)

What do you think?

Because of the extremely fast rate, the treating physicians thought that this was atrial fib with WPW.  However, this is clearly a misdiagnosis.

When the rate is so fast, it is possible to mistake a regular rhythm for an irregular one.  So one should use calipers (or mark a piece of paper and use it as calipers).  If one does this, one finds that this is perfectly regular.

Atrial fibrillation is ALWAYS irregular. This cannot be atrial fibrillation.

Furthermore, Atrial fibrillation with WPW always has polymorphic QRS complexes.  These complexes are all the same.

What is the morphology of these QRS complexes?

They are perfect LBBB complexes:  a sharp initial r-wave followed by a an S-wave that has a rapid depolarization.  The rS duration is about 55 ms, which is very short (fast) and indicates that this is a supraventricular rhythm.

Here are V2 and V3 magnified:

The initial r-wave is about 30 ms.  If this were VT or antidromic AVRT, the r-wave would be greater than 30 ms.

The rS is about 55 milliseconds.
If VT, it would be greater than 70 ms.

So this is a regular fast non-sinus rhythm with LBBB.  It is thus either:
1) PSVT or
2) atrial flutter with 1:1 conduction, or 
3) as Jerry Jones writes below, is a bundle branch block tachycardia.  This would explain the very rapid rate and also the initial fast depolarization.  Any fascicular or bundle branch VT can look just like SVT because they initiate in the conducting system.  

Pendell wrote a great post on Palpitations of unusual etiology-- all about fascicular and BB tachycardias.

In either of the first 2 situations, the conduction through the AV node is very fast.

PSVT may be AVNRT (re-entrant circuit entirely within the AV node) or may be due to WPW.  In WPW, the circuit can be down the AV node, then up the accessory pathway (orthodromic) or opposite (antidromic); re-entrant regular rhythms using an accessory pathway are called AV reciprocating tachycardia or AVRT.

If the AVRT is orthodromic, the ECG looks like AVNRT.  If antidromic, the initial part of the QRS is wide (analogous to a delta wave), not narrow, and can mimic VT.

Case 1 in this post from May 9, 2011 is a case of antidromic AVRT:

Wide complex tachycardias: 2 cases. What is the diagnosis and management?

Thus, in this case today, even if WPW is present, conduction is not via an accessory pathway; if it were, there would be a wide initial deflection, just as with VT.

Here is the ECG after electrical cardioversion:

Sinus rhythm, perhaps one PAC, nonspecific ST-T wave abnormalities.
There is no delta wave and a normal PR interval, though absence of delta wave does not rule out WPW.

A formal echo showed 37% EF, no wall motion abnormalities, but because of decreased EF, an angiogram was done and showed a 70% LAD lesion but no explanation for the dysrhythmia.

Outcome

An EP study confirmed atrial flutter with 1:1 block. It was ablated.

Discussion

Concealed conduction (not present in this case)

When an accessory pathway is present, and is resulting in dysrhythmia but is not seen on the ECG when the patient is in sinus rhythm, it is often called "Concealed conduction." 

Here is a case with Concealed Conduction and a Thorough explanation:

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

Adenosine was the appropriate initial therapy, but did not work.

Electrical cardioversion was the appropriate next therapy, and it did work.

But the diagnosis of atrial fibrillation with WPW was not correct, and this could have had consequences for the subsequent inpatient management.

The patient will get an EP study, but this has not been done yet.

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

MY Comment by KEN GRAUER, MD (6/9/2020):

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

==========
NOTE (6/13/2020): Both my comment, and Dr. Jones' remarks were made before we knew "the Answer" to this case (that Dr. Smith has just now added near the end of his remarks under, "Outcome"). So please read our remarks keeping in mind that we did not yet know "the Answer" to this case (ie, results of the EP study that was done).

==========

One of the most common and important acute arrhythmias that the emergency care provider encounters is assessment of the patient who presents with a regular WCT ( = Wide-Complex Tachycardia) rhythm. This is the focus of today’s case. I’ll add a few points to the concise explanation by Dr. Smith:

• We are not told the patient’s age, nor his previous medical history. All we know is that the patient in this case presented with non-specific symptoms — and the ECG that I’ve reproduced in Figure-1. To our knowledge — the patient was not on antiarrhythmic medication at the time ECG #1 was done.
• The rhythm in ECG #1 failed to respond to 6mg, followed by 12mg of adenosine. The patient’s BP was reported at 94/75 mm Hg. The pulse rate of 127/minute that was obtained on arrival in the ED clearly did not reflect the rapidity of his heart rate (Perhaps only every-other-heart beat produced a palpable pulse ...?).

Figure-1: The initial ECG in today’s case (See text).

My THOUGHTS on ECG #1: I’ve previously reviewed my approach to the regular WCT (ie, My Comment in the April 15, 2020 post on Dr. Smith’s ECG Blog) — as well as to the regular SVT rhythm (ie, My Comment in the October 16, 2019 post). The KEY to time-efficient diagnosis and management of these regular tachycardias is to systematically apply the principles emphasized in those 2 prior posts:

• 1st Priority — is to always determine IF the patient is hemodynamically stable. This is because IF the patient is not stable — then it no longer matters what the rhythm is, because immediate electricity is the treatment of choice for a tachycardia that produces symptoms as a direct result of the rapid rate. Despite the extremely rapid rate in ECG #1 — there presumably was at least a “moment of time” to contemplate the rhythm, because the patient was still maintaining a systolic BP of 94 mm Hg (which is a low but not critical BP), and the description of having “non-specific symptoms” sounded like he was probably still tolerating the rhythm. That said, this is clearly a situation in which, “Ya gotta be there” — as the BEST way for ongoing assessment of whether immediate cardioversion is or is not needed.
• As per Dr. Smith — Adenosine was the appropriate initial therapy, but it did not work. Given the extremely rapid rate and suboptimal BP — electrical cardioversion then became the next appropriate therapy, and it did work!

Back to the Rhythm for ECG #1: As per My Comment in the 10/16/2019 and 4/15/2020 posts — I find it easiest to assess any cardiac rhythm for the 5 KEY parameters by remembering the saying, “Watch your Ps, Qs and the 3 Rs”. I like to alter the sequence in which I assess these parameters depending on which parameter(s) is easiest to detect:

• In ECG #1 — the rhythm is regular — extremely fast — the QRS complex is extremely wide (ie, ~0.15 second) — and sinus P waves are absent. This defines the rhythm as a regular WCT.

Looking closer at the 5 KEY parameters:

• It is challenging to determine QRS width for this tracing. I thought the limits of the QRS complex in ECG #1 were best defined in simultaneous leads V1, V2 and V3. The vertical RED line in these leads shows what I took for the onset of the QRS complex. The vertical BLUE line shows my take for the end of the QRS. Continuing these vertical lines straight down to the simultaneously-obtained long lead II rhythm strip shows these limits for onset and offset of the QRS complex in lead II. This allowed me to define the onset and offset of the QRS in simultaneous leads I, II and III (vertical RED and BLUE lines drawn in those leads). I measured QRS duration as ~0.15 second.
• Sinus P waves are clearly absent in ECG #1. Several deflections that might be construed as representing some form of atrial activity are seen in a number of leads (RED, PURPLE and BLACK arrowheads in Figure-1). The purpose of my drawing those RED and BLUE vertical lines in leads I, II and III is to show that each of those arrowhead deflections falls within the QRS complex. I therefore thought those deflections were part of the QRS. I did not think there was evidence of atrial activity in ECG #1.
• One KEY to assessing the rhythm in ECG #1 — is to accurately determine the heart rate. When the rhythm is fast and regular — the Every-Other (or Every-Third or Fourth) Beat Method allows rapid and accurate rate estimation. Find a part of the QRS complex that begins on a heavy line. In ECG #1 — I chose the little spiked deflection in lead aVF (See the 1st short RED line in this lead, that appears just above the spike). Using the Every-Fourth Beat Method — the amount of time that it takes to record 4 beats (RED numbers in lead aVF) is just over 4 1/2 large boxes (BLUE numbers in this Figure). Therefore — ONE FOURTH the rate is a bit faster than 300/5 — or in this case, 1/4 the rate is ~67/minute.
• The actual rate for the rhythm in ECG #1 is therefore ~67 X 4 ~268/minute. Knowing the actual rate of the WCT rhythm in ECG #1 is relevant to this case — as we will see below.
• CLICK HERE — if interested in brief video review of this Every-Other-Beat Method.

Putting It All Together:

• The rhythm in ECG #1 is therefore a regular WCT rhythm at ~268/minute, without clear sign of atrial activity. Statistically — at least 80-90% of the time, this description for the rhythm will turn out to be VT (Ventricular Tachycardia). That said — QRS morphology in ECG #1 (as per Dr. Smith) is perfectly consistent with LBBB (monophasic R wave in lateral leads I and V6; predominant negativity in each of the anterior leads).
• Although hemodynamics are far from infallible (ie, I’ve seen cases of VT with systolic BPs approaching 200 mm Hg) — the fact that this patient remained surprisingly stable despite a heart rate ~268/minute adds support to the QRS morphology appearance that this regular WCT is likely to be supraventricular.
• So — IF the rhythm in ECG #1 is supraventricular — What kinds of SVT rhythms attain heart rates this fast? Das & Zipes (Electrocardiography of Arrhythmias; Elsevier, Philadelphia, PA, 2012) say that reentry SVT rhythms (ie, AVNRT and AVRT) most commonly do not exceed ~250/minute in adults — BUT — on occasion they can attain SVT rates as fast as 280/minute. Another possibility could be AFlutter with 1:1 AV conduction (as in a patient with WPW).

BOTTOM Line: Realistically — it’s not possible to be certain of the etiology of the regular WCT rhythm in ECG #1 from this initial ED tracing (especially given the lack of historical information about this patient). My "hunch" — is that the rhythm in ECG #1 was AFlutter with 1:1 AV conduction because: i) The ventricular rate of 268/minute is within the usual expected atrial rate range for untreated flutter (which is ~250-to-350/minute) — whereas 268/minute is faster than the rate usually seen with AVNRT or AVRT; and, ii) We are told there was no response to 2 doses of Adenosine — and both AVNRT and AVRT usually respond to this drug. On the other hand — AFlutter won't be converted with Adenosine. That Said — we can not be certain which of the above possibilities is the true etiology of ECG #1 (AVNRT or orthodromic AVRT with lbbb aberration; antidromic AVRT; antidromic AFlutter with 1:1 AV conduction, presumably with WPW — or even VT with a morphology simulating lbbb).

• What can be said (as per Dr. Smith) — is that the absolute regularity (and consistent QRS morphology) for the rhythm in ECG #1 rules out very fast AFib with WPW.
• What can also be said — is that initial use of Adenosine as a diagnostic/therapeutic trial was appropriate, especially given our suspicion that the rhythm is likely to be supraventricular. Even if the rhythm turned out to be VT — the ultra-short half-life of Adenosine (which is less than 10 seconds) makes it unlikely that the drug will be harmful.
• P.S.: We are told that the rapid rhythm in this case "was not converted by 6mg, then 12mg of Adenosine". Although it is implied by this wording that administration of Adenosine had NO EFFECT at ALL — that is not explicitly stated. I've learned the "hard way" — that one should go back to precisely what happened (in this case, ongoing monitoring strips of the inital fast rhythm during and immediately after administration of Adenosine) — to see IF there was any slowing at all — or perhaps "telltale" momentary conversion to sinus rhythm, with rapid resumption of the WCT rhythm. Even when Adenosine does not convert an SVT rhythm — it can often provide much diagnostic information by revealing hidden atrial activity during the brief period of temporary slowing after giving the drug.

ADDENDUM (June 9, 2020 @ 5pm): After writing My Comment above — I pondered this case some more. At the time I wrote My Comment yesterday — the post-conversion tracing was not available to me.

• As per Dr. Smith — the post-conversion tracing showed sinus rhythm with a narrow QRS complex; early transition (R=S for the tiny QRS complex in lead V1); and nonspecific ST-T wave abnormalities that did not look acute. There were NO delta waves. While this does not entirely rule out the possibility of WPW — it does make anterograde AFlutter with 1:1 AV conduction in a patient with WPW far less likely.

I sent the tracing and my questions to Dr. Jerry Jones, an internationally known and widely published clinician-educator, who is a frequent commenter on Dr. Smith’s ECG Blog. I think Dr. Jones’ impression, that the rhythm in ECG #1 is BBR VT (Bundle Branch Reentrant Ventricular Tachycardia) makes the most sense for the particulars of this case.

• BBR VT is an uncommon form of VT. CLICK HERE — for an excellent review of this topic.
• Dr. Smith indicates that an EP study is pending. I look forward to seeing the results!

Dr. JONES Wrote the Following to Me:

What a really interesting WCT! Here are my thoughts ...

• First, the rate — while not too fast for SOME ventricular tachycardias — it is simply too fast for MOST of those arising in the ventricles (but not ALL — more of that in a moment). I usually expect to see VTs between 160 and 180/minute — and, in my experience, most are. The rhythm is mathematically regular, so atrial fib is out of the equation. Personally, I think 268/minute is too fast for anything involving the AV node except in babies and possibly young, very healthy people. Again, we don't know the age or patient's overall condition here.
• I think a blood pressure of 94/75 mm Hg, with pulses that are only palpable about every second beat is very worrisome. A systolic BP of 94 may be OK for a woman who weighs about 90 lbs — but I am guessing that wasn't the case here. And if the patient's “normal” BP was closer to 160 — then this is a very significant drop. Again, as you say Ken: "You gotta be there!" I probably would have been inclined to go directly to cardioversion unless the patient looked exceptionally good (but again, I wasn't there). I've treated patients who have had both adenosine and sedation/cardioversion — and they ALL preferred the sedation/cardioversion!
• Regarding the issue of the smooth, straight downslope of the S wave in lead V1 — I remember a number of years ago when I first came across Marriott's famous article on how to differentiate ectopy from aberrancy, and learned about the straight, smooth downslope in V1. I was very impressed with that information, and promptly misdiagnosed a number of VTs using that finding. I found out that a VT can present with the same smooth slope — as I feel it does in this particular case. I now consider this finding supportive — but I would be very, very careful basing a diagnosis on that alone. That's like the "rabbit ears" in RBBB. Most people know that if the left ear is taller, then that represents ectopy. What they DON'T know is that the discussion ends right there — because a taller right rabbit ear can be seen in BOTH aberrancy AND ectopy.
• Finally — If the WCT in today’s case was due to antidromic conduction in a patient with an accessory pathway — then I’d expect to see evidence of ventricular preexcitation on the post-conversion ECG. But it’s not there ...

In Summary — I think the rhythm in today’s case is most likely a Bundle Branch Reentrant Tachycardia. That's why it did not respond to the adenosine — but responded immediately to the electrical cardioversion. Bundle branch reentrant tachycardias can present with a LBBB or RBBB morphology.

• In my experience, LBBB is much more common and looks often (though not always) exactly like LBBB in V1. When it begins in the right ventricle, it begins within the conduction system, coming DOWN the right bundle branch (just like in LBBB) — then crosses the septum (just like in LBBB) — and then travels back up the left bundle branch. Therefore, it is quite possible for a BBRT with LBBB morphology to have a smooth, straight downward slope of the S wave in lead V1.
• BBRTs are also well-known for their rapidity — sometimes in the upper 200's and approaching 300/minute! Hence, their lethality.

Again, I think this is most likely a BBRT with LBBB morphology. I congratulate the ER team on saving this man's life!

— Jerry W. Jones, MD, FACEP, FAAEM —