Wolff Parkinson White Syndrome on ECG – WPW Pathophysiology

Wolff Parkinson White Syndrome on ECG – WPW Pathophysiology

okay well welcome to another MedCram
lecture we’re going to talk about wolff-parkinson-white syndrome otherwise
known as WPW and let’s talk about the conduction system so we can explain
what’s going on here so here we have the electrical conduction of the heart and
as you know the sinoatrial node is where the pacemaker usually sits up here and
it depolarizes throughout the atrium but before it goes down to the ventricle all
of these pulsations electrical conduction goes to the AV node which
sits right here basically this is the only pathway for electrical conduction
to go down into the ventricles normally and as you know this is insulated so
there’s an insulated layer here so that depolarization of the atria don’t go
down at all into the ventricle now that’s important because as you know the
AV node here only allows a specific rate of conduction to go through it there’s a
depolarization and repolarization and then a refractory period where by which
an additional depolarization is not going to be allowed in straight through
and that’s kind of a safety mechanism because as you know an atrial
fibrillation up here in the atria the atria are contracting far more than 400
beats per minute and in that situation imagine 400 beats per minute being
directly transmitted down to the ventricles I mean that would be fatal so
the AV node does serve a very good purpose in controlling that okay so you
know then that there is only one way to the ventricle well unless unless of
course you have WPW which in this situation you have a congenital
abnormality called the bundle of Kent which basically is a bridge which
connects the atria with the ventricle and so now instead of the electricity
the conduction going down and sweeping in this direction going everything’s
going to the AV node before it can go down into the ventricle now you have all
of that yes but you can also take an accessory pathway is called the bundle
of Kent and you can go down into the ventricle directly depending on what
kind of congenital abnormality this is so you can quickly see here that there’s
going to be some issues this is still happening just like it normally does but
if this accessory pathway is functional and it’s actually conducting electricity
you can see that the first thing that it’s going to do is it’s gonna excite
the musculature of the ventricle and as such you’re going to go ahead and get
depolarization of the ventricular myocardium early before it occurs
through the history Kinji system and we’ll show you what that looks like on
the EKG and that’ll make sense now because there is depolarization of the
ventricular myocardium you may see a slightly longer QRS complex so basically
if you were to look at this this is the kind of situation that you’re going to
see you’re gonna see a normal P wave but normally what you would see is you would
see a normal q r s and then a T wave right but in this situation you’re gonna
see a little bit more than that because again here’s this accessory pathway
that’s coming over and so you’re going to start to see depolarization early and
so this curving up is known as a delta wave and that is pretty characteristic
of WPW so if you see a delta wave think about WPW also notice that the PR
interval here to here is going to appear to be smaller because of this Delta wave
so let’s take a look at some real examples of what this looks like on an
EKG so this is a patient with WPW you can see right away that you’ve got this
Delta wave here it’s pretty much all over the place you can see this Delta
wave of course going in the opposite direction because we’re talking about
AVR here you can see a delta wave here you can see a delta wave and again we’re
talking about that pre excitation of the ventricle so Delta waves in front of all
of these QRS complexes here’s a nice Dell
the wave as well Delta wave as well okay so these are all delta waves consistent
with WPW okay and as we mentioned this is a congenital problem and people can
present with this at all ages as children as adults they usually have you
know symptoms of cardiomyopathy shortness of breath things of that
nature there are three areas where you can run
into problems with ventricular tachycardia the first one as we were
talking about is that this bundle of Kent which is an accessory pathway can
have rapid conduction in an antegrade fashion so you can imagine that if
somebody went into atrial flutter for instance or they went into atrial
fibrillation that all of those atrial contractions will be transmitted
perfectly through the bundle of Kent and right on down into the myocardium and
that would be a one-to-one conduction so you know that atrial flutter waves for
instance are sawtooth and they are going to be going at about 300 beats per
minute and so you can imagine a ventricular rate of 300 beats per minute
is going to lead to basically ventricular fibrillation and that could
be a fatal arrhythmia and so number one the first problem that you can run into
here is basically anterior grade conduction because there is no no
refractory period it just keeps conducting it’s like a wire basically
that’s short-circuiting it the second possibility is that some of these
bundles of Kent’s believe it or not will actually have an automatic foe site in
it just like a pacemaker and it may decide to go off and send a signal down
into the ventricle and that could cause tachycardia yeah there’s another way an
accessory pathway can cause problems sometimes these pathways can conduct
exclusively in the retrograde direction in other words not from the atria to the
ventricles but from the ventricle to the atria this is called a concealed
accessory pathway because you don’t see the typical WPW pattern of a delta-wave
and a short PR now can these cause problems absolutely for example you
could have a final atrial node depolarization causing contraction going
to the AV node going down the HISP or Kinji system and then all the way to the
end and then it signals the bundle of Kent and transmits the signal back up
and you have a reentrant tachycardia and that would be a problem
in that situation it would be narrow complex but it’d be re-entrant and it
would be going through the AV node so back and forth back and forth I think
probably one of the more testable questions that you would see on a test
regarding this is regarding specifically atrial fibrillation so what happens if
somebody has WPW and they go into afib well you know that there’s gonna be
multiple contractions going on up here greater than 3 400 500 beats per minute
and it may be very very rapid so the thing is is that these are going to be
transmitted down into the AV node which is right here but also through the
bundle of Kent into the ventricle what we don’t want to do and this is really
important what we don’t want to do is we don’t want to block the AV node if
there’s a atrial fibrillation with wide-complex because if it’s a wide
complex than we know it’s going through the accessory pathway and it’s pre
exciting down here if it’s a narrow complex completely narrow then we have
no problem giving a V nodal blockers because we know that it’s going through
the AV node but if we have atrial fibrillation with WPW and there’s kind
of a widened QRS meaning it’s using the accessory pathway then if we use a beta
blocker or if we use specifically a calcium channel blocker it’s gonna block
only this AV node and it’s gonna have no effect on this accessory pathway and in
that situation this could turn into ventricular fibrillation and death so I
think they want you to know that on tests they want to make sure that you
understand that so remember this WPW with atrial fibrillation you really want
to get them out of atrial fibrillation as quickly as possible so if the patient
is unstable you need to go to DC cardioversion basically shock okay
synchronized cardioversion okay now if they are stable then don’t use the non
dihydropyridine calcium channel blockers like virap
and diltiazem and things like that that’s just gonna make the heart rate go
faster and they may actually go into tricular fibrillation what you ought to
be using is if they’re stable then you want to use medications like
procainamide or amiodarone so that is the key now let’s go back one
more time and look at an EKG of WPW and you can see again delta waves delta
waves very short PR interval delta waves okay thanks for joining us

5 thoughts on “Wolff Parkinson White Syndrome on ECG – WPW Pathophysiology

  1. Thank you so much for the very simple explanation, almost always when I saw the WPW I was afraid from this synonym, but now at least I have few points about..🌷

  2. Confidently interpret ECGs in a systematic way and see the other videos in this course: https://www.medcram.com/courses/ekg-ecg-interpretation-explained-clearly

  3. I’ve been looking for a good WPW lecture for a long time! Got another one to add to the list of medicine videos.

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