Atrial fibrillation, you want to control
that rate. You want to control that rhythm and
decreased risk of embolic stroke. That is
your objective for management. Is that clear?
When you do these, then for the most part,
you should be able to manage your patient
effectively. How do you control the rate?
Slow down the cardiac rate by maybe digoxin.
Hold on. Now what you know conventionally
for digoxin is a positive inotrophic agent.
Think about what I just said here. A positive
inotrophic agent in this step of setting would
make no sense. Because if there was an atrial
fibrillation with increased heart rate, what
does that mean to give a positive inotrophic
agent? Is that why you have given dig? Obviously
not. So even if have nothing about digoxin
and its secondary effect and why is it so
important to give it here? Then by common
sense you know that there has been another
mechanism that comes in handy. It is the fact
it slows down AV. It slows down the AV conduction.
Is that important? Yeah. That atrial rate,
that P wave is ridicously high. So if you
are able to slow down the conduction a little
bit with dig, then it works. Is that clear?
Now digoxin of course in the setting of, let
us say a congestive heart failure patient,
then you start thinking about inhibition of
sodium-potassium pump increasing, intercellular
sodium, increasing intercellular calcium thus
bringing about positive inotrophy right there.
That makes sense for congestive heart failure.
It wouldn't make sense here. That's using
it because it's slowing down the rate. Beta-blockers?
Obviously not, that was easy. You slow down
your beta 1 and by doing so you should be able
to control that rate.
Rhythm control. How do you do this? You re-establish
your sinus rhythm. What does sinus mean to you?
Sinoatrial and that sinus rhythm was completely
irregular. Anti-arrhythmic medication such
as? Well it depends, right. It really depends.
Now at this point what I would like for
you to do from pathology? Because at some
point when you bring in the management issues
or the management administration, you
want to understand the concept first and
then maybe chose a drug that makes more sense
for that particular arrhythmia, okay. So at
this point, while you are thinking about the
SA node, you are thinking about things like
the action potential 403 with SA node. What
are they? 4, 0, 3. So what is the deep polarization
phase here for an SA node? Phase 0. Is that sodium
channel? Not for an SA node. It is the calcium
channel. Is that clear? So where is the sodium
here? In 403, phase IV because it is funny.
What does that mean? Remember it is called the
funny channel. In other words, it's the sodium
channel. So we will talk about this as we
move forward. Well let me ask you this because
at some point when you do take a look at pharmacology,
I want to make sure that we will reinforce it.
It is the fact that how is it that you
are able to control the sodium channel with
phase IV? Is it a class I drug? Good, it is
not. That phase IV granted its sodium channel.
It is not of a voltage-gated. "Really? Dr. Raj,
I don't think you know what you are talking about."
Yes, I do. That phase is 0 and let me talk to
you about another action potential? If it
is phase 01234, that is mechanical activity,
isn't it? Mechanical activities 01234.
Tell me about that phase 0, that's the voltage-gated
sodium channel. That is the mechanical activity
let us say of the ventricle. So that phase
0 in 01234. Are you picture that action potential?
Close your eyes. Here it is. That phase 0
is a voltage-gated sodium channel. That is
class I. Let it be Ia or Ib. What have you,
okay? But here in SA node, in its action
potential 403 and the sodium is in phase IV,
funny, then it is controlled by ligand-gated.
Really? Because that phase IV you control by
giving a beta-blocker. A class II type anti-arrhythmic.
All I am doing here is lying down the foundation
or should I say reinforcing the foundation.
So then we understand the pathology and how
you manage this. If at this point, if you are confused,
if you are a little frustrated or if you have
lost what I have just said, repeat what I am
telling you and take a look at your normal
physiology of two action potentials in the
heart and then take a look at anti-arrhythmic
drugs and you put all this together, alright.
Then you do electrical cardioversion. At some
point, you have to cardiovert. You have to.
Because when you talk about atrial fibrillation,
because you want to get that rhythm under control.
Decreased risk of embolic stroke. Now this
one we have mentioned a few times. You want
to use anticoagulation. You are worried about
CVA, which stands for cerebrovascular accident,
a.k.a. stroke and you could prevent this from
happening by giving a warfarin. In other words,
you are thinking about the mnemonic, well
I do. Use whatever you want. WEPT. W, warfarin,
E, extrinsic. What test are you going to use
to measure warfarin? PT/INR of course. Now,
decrease risk of embolic stroke with
CVA. CHF, well aspirin alone. Hypertension.
Age of greater than 75, diabetes mellitus
and stroke. So ultimately it is a score
that you are going to give. Now depending
on the score that you are going to give meaning
to say each one of these conditions that you
are seeing here is given a certain point.
And so therefore, wherever point that you
are going to get now in this column, then
it is going to prevent a stroke from occurring.
0 to 1, aspirin. More than 2, there is coumadin.
What is coumadin? That is your warfarin. High
risk of CVA, enlarged left atrium, left ventricular
dysfunction. So these are the individuals
that we have talked about already in which
let us say that you have atrial fibrillation
that took place for mitral stenosis. Think
about that for one second. I don't know what
you are doing. What just happened? Well that was
a patient with mitral stenosis. Why was
he talking like that? Because while the left
atrium got enlarged due to mitral stenosis.
There is an opening snap, a diastolic rumble,
the left atrium is huge. I am having hard time eating. Sound like
Marlon Brando perhaps, but left atrium becomes enlarged.
It is compressing
upon the esophagus, dysphagia and also left
recurrent laryngeal nerve, hoarseness. So what
you are worried about with that enlarged
left atrium? Development of a thrombus. Sure
you are. Left ventricular dysfunction, myocardial
infarction and if it is not working properly,
once again high risk for stroke, cerebrovascular
accident. That is the objective of this entire
slide and those are the points that you want
to keep, it's called the CHAD's point.