00:01
So, now,
we can look at a ventricular myocyte action potential.
00:07
So, this is not a pacemaker.
00:08
This is the ventricular myocytes,
the ones that do all the work.
00:13
So, not the pacers,
the ones that do the work.
00:16
All right.
00:17
So, here, we start off with what -
I know it's the heart.
00:22
We started with four.
00:23
Why do we start with four?
I don’t know.
00:25
We start off with four.
00:26
That’s how they’re always going to term it.
00:28
So, you have to know it.
00:29
They start with 4.
00:30
Four is resting membrane potential.
00:34
But notice,
for a ventricular myocyte,
the line is flat.
00:40
There's no spontaneity in phase 4.
00:45
Phase 4 is flat.
00:47
It doesn't slope up.
00:49
So, there's no way it's going to reach potential on its own.
00:52
It needs to be stimulated to cause an action potential.
00:56
What is it stimulated by?
Well, pacemaker cells.
00:59
Pacemaker cells send that signal,
propagate it down throughout the heart
and that will cause the ventricular myocytes
to want to contract
or depolarize first.
01:09
Let's look at phase -
the next phase.
01:12
If you have a signal via the gap junction
that travels through and stimulates what?
Fast sodium channels.
01:22
You get phase 0.
01:24
So, phase 0 is when the sodium rushes into the cell.
01:30
Note that phase 0 is steep.
01:33
It’s fast.
01:35
A lot of sodium travels through.
01:38
Now, that is different than phase 0 in the pacemaker cell.
01:44
That was driven by calcium.
01:46
So, there's a difference between these two cells
based upon which channels open.
01:52
So, phase 0 involves fast sodium channels,
a little bit of calcium,
and also there is this transient outward potassium current.
02:03
And that’s that little blip you see at the top.
02:06
The prolonged portion is governed by calcium.
02:11
So, this is a calcium current
that travels for a longer period of time.
02:16
That is what phase 2 is.
02:19
Phase 3 involves that repolarization,
that delayed potassium response,
and that brings membrane potential back down to phase 4.
02:31
So, it is in a ventricular myocyte that we actually get to use
all the numbers, right?
We use 4,
then we use 0,
then 1 and 2,
then 3,
then back to 4 again.
02:42
So, you didn't think we were going to skip numbers, did you?
We didn't.
02:46
We just had to get them by bringing up
the ventricular myocyte action potential.
02:53
Time ones again, the link those currents with the associated channel in the myocyte action potential.
03:00
Here we're gonna go all the way from phase 4 through 0, 1, 2 and 3.
03:07
The most important channel to link up with its associated current, is the voltage-gated sodium channel.
03:15
This is our primary item that it's engaged during threshold or phase 0, and then it's deactivated during phase 1.
03:24
Its scientitic name is NAV 1.5.
03:28
Now, besides this sodium channel, we have a couple of potassium channels to deal with.
03:34
The first one are these fast-acting voltage-gated potassium channels.
03:40
And these are really only inacted during phase 1, these are very --
in doing that transient potassium current.
03:48
The L-type calcium channel, also very important during the cardiac myocyte,
here, the L-type calcium channel or the CAV 1.2,
are activated during phase 1, phase 2, and are deactivated during phase 3.
04:05
They're most associated with the plateau portion of phase 2.
04:10
And our final current to channel correlation that we need to make sure we bring out here,
is our delayed potassium channels.
04:19
These ones are activated primarily during phase 3 to bring membrane potential down closer to baseline,
and then finally also, during the phase 4, they are active.