Non-Pacemaker Action Potential – Heart Rate and Electricity

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.