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.