palpitations. What are we looking for further?
Let's take a look at what we
have done already. What did we discuss with
PR interval? Shortened. What does that mean?
Less than 0.12 seconds. What other components
do we have of WPW? Well, the next two are
going to be combined. On that QRS complex,
you are going to have something called a delta
wave or a slurred wave. And once you form
that delta wave on the QRS complex, understands
the QRS complex actually widens. So the only
thing that you are going to find widened or
prolonged in Wolf-Parkinson-White will be
the QRS complex. The PR interval will be shortened
and you will have a delta wave. You put those
to be together, the pre-excitation syndrome,
you cannot miss this. But it begins with understanding
the foundation. It is with knowing that you
have accessory pathway pathology. If you take
a look at this ECG, I want you to take a look
at the very bottom in which you end up finding
is exactly what I just said, with your delta
wave, widening of the QRS complex in a shortened
Let us take a look at management of Wolf-Parkinson-White.
Now it is just as important that you pay attention
to how you wish to control your rate and such
with arrhythmias. It is just as important
sometimes if not more to look after those
drugs that are contraindicated. Why, is the
big question? For example, up until now we
are pretty much seeing verapamil, your calcium-channel
blocker being used in every single type of
SVTs. They included afib, atrial flutter
and we had multifocal atrial tachycardia.
Digoxin, the first time that we are seeing
that really not being used or not preferred
was with multifocal atrial tachycardia. These
drugs were used as being antiarrhythmics because
it slows things down in the heart. But why is
it that in Wolf-Parkinson, why all of a sudden
even though you want to control and manage
and you want to cardiovert, end up being contraindicated?
Because how many pathways do you have in WPW?
Two. One is the physiologic normal AV node
and the other one is the pathologic and no
delay characteristics. So, therefore, if you
were to block any impulse from passing through
the AV node, what have you done ladies and
gentleman? You have now forced that impulse
to go through to the pathologic pathway and
exacerbate the condition. No other so far
SVT has an accessory pathway like what we are
seeing here with WPW. You want to avoid calcium-channel
blocker, digoxin and to a certain extent, adenosine
as well. These are the drugs in which if you
block that AV node, you are forced to go into
your accessory pathway and you don't want
that. That must be understood. So if that
is the case in terms of the medical cardioversion
and some of these drugs are contraindicated,
then what choice are you now left with? Well,
you are left with a couple. You have electrical
cardioversion if the patient is hemodynamically
unstable or procainamide infusion if stable.
Keep that in mind. Why would you think about
even using procainamide in a patient that
has an arrhythmia? Well, procainamide is a
class I drug. Stop there. Class I antiarrhythmic
is a sodium channel blocker and you have three
subtypes of class I. Ia, Ib, and Ic. Ic is
relatively simple. Flecainide is what you
are thinking perhaps and it does not distinguish
between which gate of the voltage-gated sodium
channel? What does that mean? A flecainide
can either or class IC can block the activated
channel or it can block the inactivated channel.
When you block both of these gates of the
channel, then your sodium channel for what intended purpose is
completely rendered dysfunctional.
If you do not have a voltage-gated sodium channel,
how in the world are you going to have what
phase? Zero. Phase 0 of which action potential?
The one with the plateau. 0, 1, 2, 3, 4.
That is the mechanical one. So if you can’t
have phase 0, how in the world is heart supposed
to pump? It doesn't. Are you worried about
sudden cardiac death with 1c? Yes, you are.
Let us talk about procainamide. Procainamide
is Ia. Ia used the atria advantage
because that A then represents to you the
activation gate of the sodium channel. Normally
speaking at RMP. Let us say at approximately
negative 90 resting membrane potential, what
did your sodium channel look like? Close your
eyes. Think about what it looks like. The
activation gate is closed and the inactivation
gate is opened, is it not? Where is my inactivation
gate? How important is that? Really important.
It is facing the inner side of the cell membrane.
Well, that activation gate gets opened when
it is triggered and sodium rushes in. That
is where procainamide works. Procainamide
is a 1a class in which it blocks the activated
channel, A and A. Use this as a cardioverter
if your patient is hemodynamically stable.
If not, electrical cardioversion. WPW is what
we are talking about. What are three major
components? You begin with PR interval, shortened
or prolonged, please? Shortened. What does
that mean? Less than 0.12 seconds. Move on.
QRS complex, give me the two components there.
One with the delta wave which is a slurred
and the widened QRS complex. 1, 2, 3 for WPW.
Do you ever use digoxin? No. Because then
you are forcing it to the accessory pathway.
Now, definitive treatment is
ablation of the accessory pathway. Is that
clear? These are important steps for management.
What drugs to avoid at all cost? What
kind of cardioversion, depending as to the
status of your patient and then definitive
therapy. Get rid of the accessory pathway, ablated.
Now, with our other supraventricular tachycardia,
I am just going to mention a few things here.
Now we ask them to go AV nodal reentry tachycardia
and we have atrial tachycardia. I am not going
to go into great detail about AV nodal reentry
tachycardia at this juncture, but atrial tachycardia,
ASV and SVT, would then mean that the P waves
are increasing in number. Increased heart
rate. And all that the picture is showing you
is another type of reentry of AV nodal. At
this point, I will consider this to be a little
bit too much detail, but nonetheless, I have
placed it here so that you understand ladies
and gentleman, that not only could you have something
like Wolf-Parkinson-White syndrome has an
accessory pathway, but then as you further
along into education, you will learn more
about these reentry tachycardias. One are
be prepared versus being shocked. On your
own time, you may take a look at this. Let us continue.