Discussion for 17 year old male CC: Chest pain and palpitations – WPW Part II

This is Part II of the discussion for 17 year old male CC: Chest pain and palpitations. You may wish to review Part I of the discussion.

As we covered in Part I, our patient was experiencing the life threatening combination of Wolff-Parkinson-White (WPW) and atrial fibrillation.

The EMS 12-Lead Blog team broke this conclusion up into two parts due to the importance of understanding this particular dysrhythmia. The patient survived in spite of the treatment provided, however, with the proper education both in-hospital and pre-hospital providers can rapidly identify and appropriately treat WPW and atrial fibrillation!

We also discussed that the danger in this arrhythmia is that the AV node no longer provides an effective "speedbump" for the barrage of atrial impulses. Any treatments which further slow or block the AV node without also slowing or blocking the accessory pathway will likely be lethal.

Thankfully, there are some key findings in WPW and AF which pre-hospital providers can use to identify this arrhythmia:

  • Bizarre, constantly changing morphologies due to varying preexcitation

  • If the rate meets or exceeds 300 bpm, or less than or equal to one large box, an accessory pathway must exist
  • If the rate exceeds 260 bpm, you can be confident an accessory pathway exists
  • If the rate exceeds 220 bpm, you need to be suspicious of an accessory pathway

Remember, slowing down the AV node in patients with uncontrolled atrial foci–such as atrial fibrillation or flutter–can be lethal! Stick with cardioversion or procainamide. The following, striking 12-Lead is from  a 59 year old female with palpitations (from the amazing Harvard WaveMaven case files):

Once you've seen it, you can't forget it!

However, as noted in Part I, not every patient with an accessory pathway will present with atrial fibrillation. Often they will present with a regular supraventricular tachycardia with either a narrow or a wide complex.

In the case of a regular, wide complex rhythm without discernable atrial activity treat as per ventricular tachycardia. However, it bears repeating that at rates exceeding 220 bpm an accessory pathway may be present, so avoid lidocaine and amiodarone and favor procainamide or cardioversion.

In the case of a regular, narrow complex rhythm treat as per SVT. Some of these patients may be very young, however, this should not keep you from treating them if they are unstable.

Adenosine is safe and effecacious for the treatment of SVT in children. However, vagal maneuvers can be particularly successful. With infants you can place an ice pack on the bridge of their nose to stimulate a vagal response. In older children ask them to blow through a small syringe or straw.

  • Accessory pathways, like WPW, can cause conduction rates to exceed 250 bpm and sometimes exceed 300 bpm
  • Without the speed limits imposed by the AV node, accessory pathways which receive no innervation to control them may allow lethal arrhythmias with the drugs
  • Cardioversion is a safe and effective treatment for unstable or potentially unstable tachyarrythmias such as WPW and atrial fibrillation


  • FB says:

    What about the use of adenosine for the regular wide complex tachycardia. If there is antegrade conduction through the bundle of kent and retrograde conduction through the AV node would adenosine still work in terminating the tachycardia? Even though its wide?

  • Christopher says:

    That is correct, in a regular wide complex tachycardia due to an antidromic pattern, the AV node is part of the circuit required to sustain the tachycardia! Thus adenosine will terminate the tachycardia.
    Great point!

  • Eff Dogg says:

    Ok, people are saying procainamide is OK. Why? It works on Na+ channels just like Lido. Procainemide can be proarthymic just like amio. Is the difference because proc has less effect on the AV than amio?

  • Christopher says:

    Eff Dogg,

    Procainamide is recommended in WPW because it increases the refractory periods of both the AV nodal tissues and the accessory pathway (AP) tissues (and I believe the His tissues as well). Amiodarone has not been shown to do the same and in many case reports has been shown to allow 1:1 conduction through the AP.

  • Brooks Walsh says:

    Great case! I'm going to point my residents over to this discussion.
    Eff dog, if you want a summary on the procainamide/WPW issue, check out an article here about that. Some folks think that much of the effect of amiodarone is due to beta-blocking activity, explaining why, as Christopher says, accessory pathway conduction is enhanced – not what you want to have happen!
    One thought about using adenosine for a WCT in a patient known to have WPW: while AV nodal conduction would be interrupted, many cardiologists maintain that procainamide is the drug of choice. I know that Stephen Smith believes that "no proof is neccessary" regarding the safety of adenosine in this context, but I've always been a little wary of using that line of reasoning in medicine!

  • Brooks,

    I believe Dr. Smith's point is when you're uncertain if a regular WCT is due to an accessory pathway, the mechanism would still have to be from a reentry circuit thru the AP, thus adenosine can be safely used to terminate it.

    Although, I'd wondered about atrial flutter with antidromic conduction, since functionally that is an automatic atrial focus as far as the ventricles know, however, the answer In Phibbs' text and Marriot's text is that while conduction will now prefer the AP, restoration of the AV node after the adenosine wears off will provide for competitive impulses that will eventually supersede the AP node conduction.

  • Sam Pinzon says:

    Great article. Great Information on WPW A fib. Knew about cardioversion but procainamide surprised me. Question though how does treatment differ from LGL? And how about treating brugada syndrome?

  • Sam Pinzon,

    For LGL, you have a short PRi without any sign of preexcitation where the bypass tract skips the AV node and connects directly to the His Bundle (a so called Atrio-His connection). In these patients you would simply treat the tachyarrhythmia present. I'm not aware of any specific differences in LGL from your usual SVT treatment.

    For Brugada syndrome, there is no accessory pathway in place. Instead a mutation in the patient's ion channels causes a propensity for ventricular arrhythmias. When EMS is called to "treat" a patient in this instance it may be after a syncopal episode, aborted cardiac arrest, or suddent cardiac arrest. Prophylactic treatment requires implantation of an AICD.

    I hope this helps clarify things!

  • Mark Younger says:

    Great strips. When you know that the patient has pre-excitation prior to the arrhythmia, the tachycardia should not be called "SVT" as this implies AVNRT. The correct name is orthodromic reciprocating tachycardia. You have a very good example here. The P wave will always be about midway between the QRS as with this rhythm, the ventricle and atria will never depolarize at the same time as the reentry loop will reciprocate between the two.

  • Eff Dogg says:

    Thanks guys

  • Mark Younger says:

    Something Christopher said in regard to atrial flutter being an automatic atrial focus. It must be understood that atrial flutter is NOT due to an automatic focus. Almost all cases of atrial flutter are due to a specific reentry loop in the atria. The common form called "typical" or type I flutter is technically called "counterclockwise isthmus dependant right atrial flutter".  It has a very characteristic appearance. Negative F waves in the inferior leads, F wave rate about 300. This is one of the most common rhythm problems that the clinical electrophysiologists deal with. The treatment is the ablation of the caval-tricuspid isthmus. It is often curative. Many of the ECG books that the nursing and paramedic students use are about 30 years outdated. If your book shows most tachyarrhythmias due to rapidly firing ectopic foci of automaticity, you need to throw the book in the trash.

  • Mark,

    To clarify my point, I meant functionally to the ventricles as an AV nodal blocker would not terminate the macro-reentry circuit in the atria. Your comments are well received though and I apologise if it causes any confusion! 

  • Mark Younger says:

    You are correct

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