This particular SVT is WPW. So we have now
completed our discussion of multifocal atrial
tachycardia. I have noted to you the specific
points that distinguish it from the others.
In WPW, take a look at this heart and right
off the bat, it explains everything that we
need to know for WPW. We began this discussion
some time ago. We will continue repeating
this and now we have the following discussion.
First and foremost, you are paying attention
to the green electrodes in the heart, in other
words those nodal areas where the green becomes
quite important. This is normal, the green
of the SA node in the right atrium and then
travels with the AV node. You see the cicuit
right there. You see the green node. That
green node represents the AV node. Every single
impulse originating from the SA node should
travel through there. There should be a little
bit of delay. I am purposely emphasizing delay,
why? In a little bit, there are certain drugs
that you want to avoid at all costs in WPW
and that point of me reiterating delay is
huge. Now where the pathology is what you
are seeing shaded in the brown. That is an
accessory pathway. That pathway should not
be existing ladies and gentleman because that
pathway exists that pathway right there does
not have the characteristic feature of being
able to delay your impulse traveling from
the atria down through your ventricle. Now
what I am going to do is get straight to the
clinical points because you can spend hours,
days, weeks, what have you on WPW. We don't
have the luxury of that kind of time. All
we can do at this point is simply figure out
this is my patient walking in. Take a look
at the EKG, no doubt. It is WPW. And then after that,
you get into as much detail as you wish. Education
is as you know endless and it is absolutely
enriching, but you must lay down the foundation
first. So that pathway, accessory as you are
seeing there in the brown shaded area is what
you are paying attention to. It's not, it
doesn't have the delay characteristics, so,
therefore, any impulse have might then travel
through it, guess what? It is going to go through it
way too quick. Listen to what I just said. It
passes through there too quickly. So what does
that mean to you clinically? What does that
mean to you in terms of an investigation known
as your EKG? It is the fact that your electrocardiogram
where an impulse from the SA node may then
be traveling through your atria and then into
the ventricle too quickly is what is that
by definition? PR interval on EKG. So that
PR interval once again you tell me what normal is.
The time is 0.12 seconds or 120 milliseconds
to 200 milliseconds a.k.a. 0.2 seconds. Right? If it
travels through that too quickly, what have you
done to the PR interval? Good. Shortened it. Is that
clear? Completely the opposite of what? AV
block. All those AV blocks that we talk about
ladies and gentleman that PR interval we know
mostly those PR intervals in AV blocks were
prolonged. What is the one big exception?
Mobitz type II under second-degree AV block.
You remember that. If you don't my big attempt
to make sure you review that. This is the
time to solidify and distinguish each one
of your arrhythmias. So far your focus is
where? On that shaded area, that accessory
pathway, impulse traveling through there too
quickly, our first real diagnosis where the
PR interval has been shortened. Are we good? Less than
0.12 and that is what you are looking for.
Next well what is this called? It is called
the bypass tract. You call this as a pre-excitation
syndrome. So if by chance, you don't see the
term WPW, Wolf-Parkinson-White, then the other
names for this would be a pathologic accessory
pathway disease or a pre-excitation syndrome,
which is exactly what it is. Now, are we done?
So far we have one component of WPW. There
are going to be two others and those two will
be related as we shall see moving forward.
How would one develop WPW, Wolf-Parkinson-White?
A congenital issue. What is happening? Instead
of the impulses traveling through the AV,
it will then bypass. Bundle of Kent is something
that you want to keep in mind anatomically
please, memorize that, causing earlier ventricular
activation. What happens to your PR interval?
It gets shortened. It is one pre-excitation
syndrome. Keep in mind. As you move on into
subspecialities or specialization in general,
you will talk about many reentry, but,
at least know one before this course is over
and note well. It could be associated with
afib. Imagine reentry, a circle. You are
not going anywhere and you keep come back
in the atria. The atria doesn't know how to respond.
So, therefore, may lead into atrial fibrillation.
Atrial flutter or hypertrophic cardiomyopathy,
so it could result in many issues, beginning
with WPW. Ebstein's anomaly of the tricuspid
valve, well with this especially with the lithium.
We have a patient who mighty have bipolarism
is taking lithium and lithium, a number of theories out
there, remember as far as medicine is concerned
for the most part, if it comes to actual official
questions or if people are looking for actual
definitive and confirmation, it is not based
on theory, it has to be confirmed. So you
can take a look at the number of theories
in terms of mechanism action, please do so.
But there is one that you definitely want
to know for lithium and it is the fact that
there was a side effect Ebstein's anomaly,
but, more importantly, lithium works down
in the collecting duct.
And so therefore, one of the things that
you are worried about lithium is the fact
that it could result in what kind of issue?
It would be lithium toxicity in two different
places either tricuspid in the heart and please
do not forget, lithium toxicity when dealing
with the kidney as well. And down the kidney,
lithium in the collecting duct principle
cells, it can replace that sodium channel.
So I want to go down to collecting duct. This
is important. Pay attention and that lithium,
we are doing everything at the same time, integration.
The lithium then substitues the sodium channel
of the ENAC on the apical membrane. Are you
there? Apical membrane facing the urine. Lovely
place to be. Look at the urine passing through.
That is where ENAC is. The sodium channel
could be replaced by lithium and if it accumulates
inside your cell enough, you could have damage
to the kidney because it is not a substitute
for the sodium of the sodium-potassium pump.
If I were you at this point, I will switch over
to lithium and make sure that you understand
the two major toxicities up in the heart with
the tricuspid known as Ebstein and then down
in the kidney where you might have lithium
toxicity. This would be a good time to
do it, ladies and gentleman. Let us continue
wtih WPW. So we have palpitations,
I really could have repeat this any further.
It is the fact that once your heart starts
getting disregulated that you are not having
proper cardiac output. There is no proper
organization of blood flow. So, therefore,
resulting in dizzziness, syncope, not good,