Re-entry

[FL_Medic]

In a pt. with WPW we are aware that cardizem is contraindicated because of the detrimental effects it can cause.

In pt.s with WPW you have that extra electrical pathway between the R atrium and R ventrical. If this rythm becomes rapid as a result of re-entry and we push a calcium channel blocker it causes that extra pathway to take over and the pt. can decompensate into a worse rythm. My data on this may not be exact I am trying to remember this from school so bare with me.

My question is if you have a re-entry problem closer to the junction like we may have in some SVTs and other rapid atrial rythms. Is Cardizem proven to work? How do we know that blocking the calcium channels in other rythms will not throw the pt. into an even worse rythm?

Another question I had was if anyone has seen a 12-lead of a WPW pt. in a rapid A-fib. I have seen this once in an inservice training and was wondering if anyone knew where I could get my hands/eyes on such a 12-lead.

[Ace844]

Here's your 12-lead you requested

http://www.ecglibrary.com/wpwaf.html

http://www.ecglibrary.com/wpwaf2.html

http://en.wikipedia.org/wiki/Wolff-Parkinson-White_syndrome

http://www.clevelandclinic.org/heartcenter...mp;thirdCat=259

Treatment of AFib associated with WPW is necessarily different than for a patient with a normal heart. AFib is an irregular rhythm as opposed to the regular rhythm seen in CMTs.

The basic treatment principle in WPW AFib is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. This is in direct contradistinction to the goal of treatment of non-WPW AFib, which is to slow the refractory period of the AVN.

If AFib were treated in the conventional manner by drugs that prolong the refractory period of the AV node (eg, calcium channel blockers, beta-blockers, digoxin), the rate of transmission through the accessory pathway likely would increase, with a corresponding increase in ventricular rate. This could have disastrous consequences, possibly causing the arrhythmia to deteriorate into V fib.

Thus, standard treatments for non-WPW AFib must be avoided and replaced by cardioversion with the possibility of procainamide as a potential medical therapeutic alternative. Patients presenting with Afib in WPW syndrome are typically very tachycardic and often hypotensive with evidence of hypoperfusion, thus given this unstable state, primary synchronized cardioversion should be the first-line treatment.

If the patient is stable, medical therapy with procainamide may be tried. Procainamide (17 mg/kg IV infusion, not to exceed 50 mg/min; hold for hypotension or 50% QRS widening) blocks the accessory pathway, but it has the added effect of increasing transmission through the AV node. Thus, although procainamide may control the AFib rate through the accessory pathway, it may create a potentially dangerous conventional AFib that may require treatment with other medications and/or cardioversion. Prompt cardioversion of patients with WPW syndrome and AFib may be required for any patient who is deteriorating or failing to improve.

Medical management may be a viable option in some patients, but it may have unpredictable results. Note that cardioversion is always the treatment of choice in unstable patients. If medical management is recommended it should be under the direction of a cardiologist.

Treatment of CMTs (regular and generally narrow complex tachycardias) associated with WPW syndrome yields several treatment approaches. Unfortunately, there is a paucity of literature and controlled studies, which makes the chosen treatment less definitively advocated. The two common approaches include cardioversion and the use of adenosine. If adenosine is chosen, all preparations for immediate cardioversion and appropriate resuscitation should be in order in the event of degeneration of the rhythm after adenosine-induced AV nodal blockade

In a stable patient with a regular narrow complex tachycardia (not known to be a result of WPW syndrome), adenosine (6 mg rapid IV push; if unsuccessful, 12 mg rapid IV push) should be the first-line treatment. (Adenosine is contraindicated in heart transplant patients and should be used with caution in patients with severe obstructive pulmonary disease and in patients with a wide QRS complex, unless the diagnosis of PSVT with aberrancy is certain.) When WPW syndrome is known or highly likely, adenosine should be used with caution and preparation for cardioversion/defibrillation should be immediately available.

Once the circus movement is broken, the patient usually converts to sinus rhythm. Note that whether the QRS complex is regular or irregular distinguishes CMTs from AFib on ECG.

If the QRS complex is regular and narrow, the arrhythmia may be treated with adenosine as if it were CMT or PSVT, as long as preparations for cardioversion/defibrillation are immediately available.

If the QRS complex is irregular, the arrhythmia is likely AFib. In this case, adenosine theoretically could increase the rate and cause clinical deterioration and should not be used.

Cardioversion, or in some cases, procainamide, are the treatment choices in these situations (ie, irregular QRS complex), providing the necessary rate control.

If in doubt about the regularity of the rhythm, it is safer to err on the side of treating for AFib in the context of WPW syndrome with direct cardioversion.

(

Goldberger: Clinical Electrocardiography: A Simplified Approach @ 6th ed.,)

Wolff-Parkinson-White Pattern

The WPW syndrome is an unusual and distinctive ECG abnormality caused by preexcitation of the ventricles. Normally the electrical stimulus passes to the ventricles from the atria via the AV junction. The physiologic lag of conduction through the AV junction results in the normal PR interval of 0.12 to 0.2 second. Imagine the consequences of having an extra pathway between the atria and ventricles that would bypass the AV junction and preexcite the ventricles. This is exactly what occurs with the WPW syndrome: an atrioventricular bypass tract * connects the atria and ventricles, circumventing the AV junction (Fig. 10.18) .

Preexcitation of the ventricles with the WPW syndrome produces the following three characteristic changes on the ECG (Figs. 10-19 and 10-20) :

The QRS is widened, giving the superficial appearance of a bundle branch block pattern. However, the wide QRS is caused not by a

--------------------------------------------------------------------------------

* Formerly called the bundle of Kent.

--------------------------------------------------------------------------------

delay in ventricular depolarization but by early stimulation of the ventricles. (The QRS is widened to the degree that the PR is shortened.)

The PR is shortened (often but not always to less than 0.12 second) because of ventricular preexcitation.

The upstroke of the QRS complex is slurred or notched. This is called a delta wave.

Figs. 10.19 and 10.20 show the WPW pattern, with its classic triad of a widened QRS, a short PR interval, and a delta wave. Notice that the pattern superficially resembles a bundle branch block pattern because of the widened QRS complexes. Depending on which area of the ventricles is preexcited first, the ECG may show a pattern simulating that of either RBBB with tall R waves in the right chest leads or LBBB with a predominantly negative QS in lead V1 .

The significance of WPW preexcitation is twofold:

Patients with this pattern are prone to arrhythmias, especially paroxysmal supraventricular tachycardia (PSVT) (Fig. 10.21) .

The ECG of these patients is often mistaken as indicating a bundle branch block or MI (see Fig. 10.20) .

The WPW syndrome predisposes patients to develop paroxysmal supraventricular tachycardia (PSVT) because of the presence of an extra conduction pathway. For example, a premature impulse

traveling down the AV junction may recycle up the accessory pathway and then back down the AV junction, and so on. * This type of recirculating impulse is an example of reentry.

Another type of preexcitation variant, the Lown-Ganong-Levine (LGL) syndrome, is caused by a bypass tract that connects the atria and AV junction. Bypassing the AV node results in a short PR interval (less than 0.12 second). However, the QRS width is not prolonged, because ventricular activation occurs normally. Therefore the LGL pattern consists of a normal-width QRS complex with a short PR interval and no delta wave; the WPW consists of a wide QRS complex with a short PR interval and a delta wave (see Fig. 10.19) .

Patients with the LGL pattern may also have reentrant-type PSVT or paroxysmal atrial fibrillation or flutter. *

And Here's 2 more images for ya.

[FL_Medic]

excelent, what search engine do you use?

[Ace844]

excelent, what search engine do you use?

LighteningFastACE search.com

Actually you just happened to catch me studying using "Zipes: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., Copyright © 2005"

ACE844

[AZCEP]

The management concerns are not only directed toward Cardizem.

Any agent that works through slowing conduction through the AV node has the possibility of worsening the tachycardia. Adenosine, Beta blockers, Calcium channel blockers, vagal maneuvers can all have negative effects on the patient. Patient tachycardic, accessory pathway noted, AV blocking agent used, tachycardia worsens.

Drugs like Pronestyl and Amiodarone, that work on atrial and ventricular tissue, are the agents of choice. Amiodarone does not do a great job, but it can work. Pronestyl has been around a long time, but few EMS systems carry it.

[FL_Medic]

The management concerns are not only directed toward Cardizem.

Any agent that works through slowing conduction through the AV node has the possibility of worsening the tachycardia. Adenosine, Beta blockers, Calcium channel blockers, vagal maneuvers can all have negative effects on the patient. Patient tachycardic, accessory pathway noted, AV blocking agent used, tachycardia worsens.

Drugs like Pronestyl and Amiodarone, that work on atrial and ventricular tissue, are the agents of choice. Amiodarone does not do a great job, but it can work. Pronestyl has been around a long time, but few EMS systems carry it.

Thanks for your input.

we carry verapakill, cough I mean verapamil... yet another dangerous calcium channel blocker I don't think we are educated enough about.

[AZCEP]

The drug, in and of itself, is not dangerous. I'd be willing to bet that right now there are hundreds of bottles of the stuff near your stations sitting in a cabinet minding their own business. Now, when they start plotting, we need to worry.

The danger is in the mind/hands of the providers that have discovered they didn't receive enough education on how to use this wonderful medication, and have not taken it upon themselves to find out what it can/can't/should/shouldn't be expected to do. Once that is taken care of, very few medications are as effective for their intended jobs as Verapamil.

[FL_Medic]

The drug, in and of itself, is not dangerous. I'd be willing to bet that right now there are hundreds of bottles of the stuff near your stations sitting in a cabinet minding their own business. Now, when they start plotting, we need to worry.

The danger is in the mind/hands of the providers that have discovered they didn't receive enough education on how to use this wonderful medication, and have not taken it upon themselves to find out what it can/can't/should/shouldn't be expected to do. Once that is taken care of, very few medications are as effective for their intended jobs as Verapamil.

Are verapamil vials are strapped with loaded guns, lol.

You're right, bad wording in my last post.