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This blog is sort of an experiment. An experiment to test my theory that most providers don't have an adequate understanding of Wolff-Parkinson-White Syndrome and its treatment… And it really began years ago when I would frequently ask nurses and medics, “If I asked you how to treat SVT, more specifically, a stable and narrow SVT (likely AVNRT or AVRT), how would you treat it?” I was always met with, “are they stable or unstable?” Then we would go down a rabbit hole of “what if this, or what if that…” and “I’d try vagal maneuvers, then…” BLAH, BLAH, BLAH! The entire reason I inquired about this was that I wanted to know how they would treat it pharmacologically. No one wanted to answer with medication, so I had to advance the question. “Gun to your head, you have to choose a medication… and if you say anything but a medication… BANG!”



I am often met with the answer, “Adenosine, duh!” But then I like to take it a step further. I ask, “OK, but what if the patient had a suspected or confirmed history of Wolff-Parkinson-White (WPW)?” Suddenly I am met with much less confidence and often very conflicting answers. So I took to FB (cause you know, that’s where the best educational advice is had) and asked this question on many EMS and nursing pages:


“SVT (presumed AVNRT or AVRT) with a rate of 200. Confirmed history of WPW. How would you treat it, pharmacologically? I’m simply interested in your opinions and why you chose what you did? Disclaimer: I know you would try ‘this or that’ first… vagal maneuvers… blah, blah, blah… Gun to your head, you have to pick a medication.”



*** These are actual responses on FB. YES, the profile names and pictures were changed to conceal identities. NO, the group "I'm in EMS, I'm Right..." doesn't exist... That I am aware of... ***

*** These are a small snippet of the 6 + webpages I posted this question on. I did post it to pages I believed would answer incorrectly, and to others that are full of reported experienced and knowledgable providers I thought would nail the treatment ***


The point of this was to see if there was any kind of consensus on the question I asked many of my peers. And honestly, I was not surprised at the answers. Some were spot on and some were far off. 

Many, after hearing the WPW word, now are NOT wanting to treat it as the same stable and narrow SVT as mentioned above (pharmacologically, at least). I am not gonna sit here and pretend I am the brilliant one for knowing this. Mainly because, many years ago, I had the same train of thought as many of the providers within the comments on Facebook above — DON’T GIVE ADENOSINE TO A PATIENT WITH WPW BECAUSE YOU WILL KILL THEM! While the thought process can in some situations be correct, It's more often than not... incorrect!  



I was misled by the opinion of other medics and medical providers in the past, which is unfortunate. But today, I see Facebook comments doing what was done to me at the beginning of my career, misleading the naive. Patients with this “WPW condition” shouldn't be approached with confusion and we especially shouldn’t be following the advice of a random provider on Facebook with very little to back up their aggressive claims. I wanted to see if I could clear some things up by answering a few questions, so here goes:


1. What is WPW

2. How do I recognize/diagnose WPW

3. How do I treat WPW 



What is WPW?

There really isn’t an answer for, “what is WPW?” It is better explained by asking the question, “what is WPW Pattern,” and “What is WPW Syndrome.” Two very different presentations.


WPW Pattern - Applies to the patient with pre-excitation manifest on the ECG in the absence of symptomatic arrhythmia. This is what clinicians often think of when they hear, “this patient has a history of WPW.”

WPW Syndrome - Applies to the patient with pre-excitation manifest on the ECG in the presence of a symptomatic arrhythmia. This is what clinicians believe can’t be given Adenosine.



Pre-excitation Syndrome - Early activation/depolarization of the ventricles due to impulses bypassing the AV node via an accessory pathway. The presence of a short PR interval, frequently with a delta wave, are seen in pre-excitation syndrome. WPW is a type of pre-excitation syndrome (but not the only one).

Accessory Pathway - Anatomic structure often referred to as the Bundle of Kent, or the Kent Bundle, or bypass tract. It is essentially a band of muscle connecting the atria to the ventricles. Again, this anatomic structure is NOT called WPW or a WPW; its a manifestation of this structure (the structure is what causes the pre-excitation seen on the ECG).



How Do I Recognize / Diagnose WPW Pattern and Syndrome?


Well…. WPW Pattern is the easy one, so let’s start there.


WPW Pattern:

  • Typically only needs a 12-lead ECG to diagnose
  • Identified by:
    • Shortened PRI (less than 120 ms or 0.12 seconds; 3 small boxes)
    • Delta wave
The shortened PR interval and Delta wave occur due to early depolarization through the accessory pathway causing pre-excitation of the ventricle. The pre-excitation, because it isn't moving through the normal conduction pathway (superhighway), occurs slowly but earlier than the normal conduction and depolarization. This earlier than normal depolarization is represented by a Delta wave. 
*** Pre-excitation causing early depolarization through the right atrium to the right ventricle via an accessory pathway *** 
This is due to the fact that that the depolarization wave from the atria bypasses the AV node via the accessory pathway (Kent Bundle) on its way to the ventricle. As the pre-excitation slowly depolarizes the ventricle, the AV node then releases its impulse -- following its normal conduction pause -- to the ventricles where the depolarization wave, through standard conduction, meets the depolarization wave through the accessory pathway. These two depolarization waves meet, then execute. 
WPW Syndrome
  • Identified By:
    • A surface ECG showing accessory pathway activation (WPW Pattern)
    • Tachyarrhythmia or episodes of tachycardia
WPW Syndrome is often referred to as SVT by many clinicians when it is seen on the ECG, as it most often appears in its orthodromic form -- Narrow, regular, and fast as hell with absent P waves. WPW Syndrome though has a variety of flavors, seen here:
Regardless of the flavor, the accessory pathway is the problem. Whether it's a re-entry loop or a chaotic mess of depolarization received from the atria due to A-Fib, we have a failure of electrical regulation due to the patient's accessory pathway. These patients, after correction of the tachyarrhythmia, will be found with an underlying WPW Pattern on the surface ECG. 
Now to ask the question, "What if, after correction of the tachyarrhythmia, you don't find an underlying WPW Pattern?" Well... Not every accessory pathway will manifest on the ECG with a Delta wave and shortened PRI. It depends on the location of the accessory pathway anatomically and if it's a concealed or bi-directional pathway. To further complicate things, WPW pattern may only intermittently present on a 12-lead ECG in patients with an accessory pathway. The best way to determine if it is WPW Syndrome is to ask yourself, "Is the morphology I am seeing on the ECG dependent on an accessory pathway?" or "Is an accessory pathway the only reason that this rhythm may exist?" If your answer is yes to those questions, then it's likely WPW Syndrome even if the underlying rhythm isn't showing WPW pattern. 
As you all likely know, it is very difficult to differentiate AVNRT from AVRT and VT from an SVT with aberrant conduction or A-Fib + Pre-excitation. I believe this to be another topic for another day, but I will leave you here with these links to freshen up your differentiation skills:
How do I treat WPW? 
Below, is a 2015 AHA Tachycardia With a Pulse Algorithm. It has been annotated by myself to assist with the decision making required when treating our patients with the dreaded WPW Syndrome. I have changed nothing regarding the actual algorithm. I simply added my thoughts to assist with the decision making and treatment of your patients who may fall into this category. You should continue to follow the "Shock if they are unstable" and "consider vagal maneuvers" guidelines before moving onto pharmacological treatment. 
Orthodromic AVRT Treatment:
This variation of AV re-entrant tachycardia is likely the rhythm you had in your head when I mentioned a narrow complex SVT at the very beginning of this blog. Treatment of this tachyarrhythmia will follow the shaded portion of the algorithm. Orthodromic AVRT is a narrow complex tachycardia where antegrade conduction occurs through the AV node with retrograde conduction occurring via an accessory pathway. This usually occurs due to an ill-timed premature contraction catching the accessory pathway in a refractory state and the AV node ready to depolarize. By the time depolarization is near completion in the ventricles, the accessory pathway is no longer refractory, allowing retrograde conduction back into the atria. This leads to early activation of the atria, thus beginning the continuous re-entry loop seen in AVRT. This is what produces that narrow complex tachycardia we all love to call SVT. 
Orthodromic AV Re-entrant tachycardia must be eliminated by putting a stop to the re-entry loop/circuit. That's where medications that affect the AV nodes refractoriness or depress it's normal conduction velocity come in. Adenosine is the most common medication used in this situation, although recently, Diltiazem has become the in vogue medication for this situation with it's higher success rates for conversion and overall comfortability offered to the patient. 
*** Sam has a lecture within the F3 Content of the FOAMfrat Paramedic Refresher covering Adenosine Vs. Diltiazem in detail regarding the termination of re-entry tachycardias *** 
As always, you should follow your local protocol regarding the treatment of any patient. Here are the general guidelines for medication administration of a patient with a narrow complex tachycardia that is a presumed orthodromic AVRT:
- 6 mg. This should be followed by a dose of 12 mg if the first dose is ineffective. 
- Given rapid IV push over a couple of seconds with a rapid flush to follow of 20 cc's or more.
- 0.25 mg/kg SIVP, over a couple of minutes
- 0.35 mg/kg SIVP, over a couple of minutes if the initial dose is ineffective.  
Antidromic AVRT Treatment:
This variation of AV re-entrant tachycardia is not likely what you envision when someone mentions AVRT, at least for me that was the case. Antidromic AVRT treatment will lead to the right side (wide side) of my annotated algorithm. Antidromic AVRT is a rhythm caused by a re-entry circuit, similar to Orthodromic AVRT, but the loop is circulating in the opposite direction. In this tachyarrhythmia, retrograde conduction occurs through the AV node and antegrade conduction occurs through the accessory pathway. This again occurs due to an ill-timed premature contraction, this time catching the AV node in a refractory state and the accessory pathway ready to transmit depolarization waves from the atria to the ventricles. This leads to early activation of the ventricles, thus beginning the continuous re-entry loop seen in AVRT. This is one of the causes of the wide complex tachycardia we all love to call ventricular tachycardia (although it's not). 
Similar to Orthodromic AVRT, Antidromic AVRT can be eliminated by putting a stop to the re-entry loop/circuit between the atria and the ventricles; But that's where things get complicated. Unlike its narrow complex counterpart, if another rhythm is mistaken for Antidromic AVRT, your choice of medications can be deadly. So the safest answers here are... Elective cardioversion or Procainamide. But if you are sure the presenting wide complex tachycardia is Antidromic AVRT (and you are 100% sure), conduction interrupting medications such as Adenosine or Diltiazem are safe. The algorithm reads, "consider adenosine if regular and monomorphic." Which, if it is regular and monomorphic... as my annotation says, "Drugs should be fine!" This would be due to the assumption that this rhythm is again, possibly monomorphic VT, SVT with aberrant conduction, or antidromic AVRT. 
If you're looking for Antridromic AVRT, try to identify these findings on the ECG
- Wide complex QRS (>120 ms), possibly with a delta wave present
- Regular ventricular rate; 150 - 250 beats per minute.
- P waves are generally not visible. 
Infusion; 20 - 50 mg/minute. Continue and monitor closely until:
- The arrhythmia terminates
- Hypotension is encountered
- QT prolongation occurs
- A total of 17 mg/kg has been given
10 minute infusion; 150 mg
 A-Fib + Pre-Excitation Treatment:
The very last thing on the algorithm is, "Consider expert consultation." This is when your rhythm is likely a wide complex irregular tachycardia. Now, it could be hypomagnesemia induced Torsades De Pointe (TDP), but I think TDP is easy to identify on the ECG and relatively simple to exclude as a possible differential; but it's a good differential to consider. That pretty much leaves, A-Fib + pre-excitation...
This is the worst combo you can have regarding WPW syndrome. The good news is, the treatment is likely going to be synchronized cardioversion due to patient instability, narrowing your treatment choices down to a quick and easy ZAP. In this presentation, conduction to the ventricles occurs both through the normal conduction pathway (AV node) and the accessory pathway. The refractory period of the accessory pathway is much shorter than the AV node, meaning that it will allow a very rapid rate of depolarization in the ventricles. The "fibrillation waves" in A-Fib can reach rates exceeding 300 waves per minute. This can lead to an unregulated, wide, and irregular ventricular rate.
The goal of drug therapy for A-Fib + pre-excitation is prompt control of the ventricular rate and, if possible, elimination of the atrial fibrillation. If the patient is "stable" you should exercise extreme caution when administering medications. As with any tachycardia patient requiring treatment, defib pads should be in place. If a drug is chosen, it should have an action that lengthens the antegrade refractoriness and slows conduction in BOTH the AV node and accessory pathway. Procainamide is effective for the treatment of A-Fib + pre-excitation due to its effects on atrial and ventricular myocardium without any AV nodal blocking effect, slowing the refractoriness and conduction of the accessory pathway, and possibly terminating the atrial fibrillation. Drugs that target the AV node and not the accessory pathway, such as Adenosine and Diltiazem, are thought to promote conduction down the accessory pathway and enhance the rate uninhibited, possibly worsening the patient's condition. 
Expert Consultation:
One phone call to a doctor -- No shame!
Infusion; 20 - 50 mg/minute. Continue and monitor closely until:
- The arrhythmia terminates
- Hypotension is encountered
- QT prolongation occurs
- A total of 17 mg/kg has been given
No longer recommended (click below)
 Summarized Treatment Reference:
I didn't do an official experiment outside of a little bit of trolling on Facebook. But I do believe I did find an answer to my question... YES, there are many providers out there who don't have an adequate understanding of WPW Syndrome and it's treatment (enough to give me the motivation to write a blog about it). BUT! I did find that there were many out there who also did, to my pleasant surprise! 
Jared Patterson, CCP-C, One Rad Medic 
Twitter @OneRadMedic
Reference(s), Bitches!

Kulig, James, and Bruce A. Koplan. “Wolff-Parkinson-White Syndrome and Accessory Pathways.” Circulation, 12 Oct. 2010,

Burns, Dr. "Pre-Excitation Syndromes • LITFL • ECG Library Diagnosis". Life In The Fast Lane • LITFL • Medical Blog, 2020,
Pre-excitation, Atrioventricular Reentrant (Reentry) Tachycardia (AVRT), Wolff-Parkinson-White (WPW syndrome) – ECG & ECHO. (2020). Retrieved 14 May 2020, from

Garcia, Tomas B. 12-Lead ECG: the Art of Interpretation. Jones & Bartlett Learning, 2015.


Making Your Presentations... Prolific!


If I click baited you into reading this with my cover art, I assume you are an educator looking to "spruce" up your presentation skills; or maybe you're a newbie looking to enter the world of teaching and education. I, too, was in the same spot, and while I think I still am a newbie, I have found many ways to improve my lectures and presentations over the years. I have been continuously trying to find ways to engage an audience, capture further and maintain their attention, and use visually pleasing slides, all while attempting to keep the information I relay easy to retain. That's where Prolific: The Speakers Atlas comes in.


Prolific: The Speakers Atlas is an online course directed at educators (or even soon to be educators) with intentions of elevating their lecture game and improving their presentations overall. Sam Ireland and Tyler Chrisitifulli are your instructors during this approximately 5-week long course, and you will find that they are handing out their "secrets" to education. 


Through emulation and a short stent through their course, I began revamping some of my content.

Lookie here:

(Slides from a capnography course I created; Eric Bauer’s “3 P’s of EtCO2) 

Not only did I improve the appearance of the slides, but through some constructive criticism from Sam and Tyler, I have learned to further appeal to the audience by using animations timed with my lecture to upgrade the entertainment value of my presentations.



As I nerd out on an almost daily basis -- and annoy the hell out of my wife --  over EMS related jumbo, I have co-workers and friends asking many questions about how I put some of my content together. I tell them about the Prolific course, of course. But I realize that it doesn't really answer the question. So here, I attempt to answer the questions I get the most often regarding the Prolific: The Speakers Atlas course. 



How do they do it?

As I mentioned… Through their course, Prolific: The Speakers Atlas. During that 5-weeks (5 online modules, at your own pace), Sam and Tyler take you through all you need to know to improve your presentations and lectures. This includes:


Content Development – This is the first module, where the course begins. The module includes material on content framework and storyboarding. You’ll learn to brainstorm ideas and allow natural progression for those ideas. You then start learning to develop a presentation and how to cater that presentation to specific time frames or different audience types. Sam and Tyler then teach you to build from your thoughts and organize the mess of ideas in your head. 

Graphic Design – In the second module, you get into my favorite part of the course: graphic design. You've watched many of the FOAMfrat presentations, I imagine. If you're anything like me, you've asked yourself, "how do they do that?"  Whether you use PowerPoint or Keynote, they got you covered.

Transitions and Builds – Imagining how your talk will go and how it actually goes when you are in front of an audience is often very different. Module three will dive into the speaker's mind and cover the avoidance of the audience divide through the clever use of transitions and builds within your presentation. You'll learn to avoid looking and feeling awkward in front of an audience.

Speaking and Drawing – Bueller? Bueller? Bueller? Module four concentrates on speech variability and avoiding that monotone voice everyone hates from presenters. You'll also dive into free drawing, memorization, and illustrations often seen on what many call, "whiteboard exercises."

Showing Up and Leaving Them Wanting More – How do we show up prepared? What awkward behaviors should we avoid? How do I keep the audience wanting more without looking like a douche? Module five covers these questions, without making you look… like a douche. Know your call to action and give the audience something to do when they leave.



Is the course stressful, is it graded?

Yes, to both, but in a good way! You’re getting two of the best speakers and educators in our industry giving you constructive criticism. Can that be stressful? Of course, but you have an opportunity only providers who take the course get; turn that stress into excitement.

You’ll have assignments, Q&A, and even a capstone project to show off all of the information you learned throughout the course. You'll be graded, but you won't fail. If you’re anything like me, you’ll be anxiously waiting for them to grade and critique your work.


While I thought this cover art was a masterpiece, following some criticism from Sam and Tyler, I learned quickly of some very common mistakes that educators make while creating their work. I’m gonna leave you wondering with this one. Take the course then come back and judge my work.




 Did you learn anything cool?

Hell yeah! I've used my obsession with memes and GIFs and found a way to include them in my presentations... THANKS, SAM!

 (Yes, they taught me to create these!)

Now, I could go on and on about the course… But I don’t want to bore you with a blog that’s too long (something they teach within the course). To summarize, take the course and let Sam and Tyler teach you some pretty rad things and improve your presentations/lectures. You’ll also gain access to an exclusive group on FB full of other EMS educators with similar passions.




Take The Course Now!




- Jared Patterson, CCP-C, One Rad Dude



Patterson, Jared M. (1989). Pretending to have an actual reference for this blog. Omaha: Nebraska. Patterson and Friends, LLC (Not really an LLC). #medicsagainst500and12. PROLIFIC2020 FOR 50% off.




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