15.  Cardiovascular Physiology (cont.)
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15. Cardiovascular Physiology (cont.)


Professor Mark Saltzman:
So, today we’re going to continue to talk about cardiac
physiology. In particular,
the electrophysiology of the heart which is quite interesting
and important to heart function. One of the–turns out that one
of the most important diagnostic measurements that can be made is
through a device that was designed by biomedical engineers
called an electrocardiograph. We’ll talk about today sort of
the origins of electrical activity in the heart,
the role that this electrical activity plays in the function
of the heart, and then finally how–we’ll
talk a little bit about how one can measure that electrical
activity which comes from cells in the heart,
sort of deep inside your body, but can be measured with
electrodes on the surface of your body.
You’ll get some more experience with making those measurements
in section on Thursday afternoon.
This is–I apologize, a rather complicated diagram,
but I wanted to show you a picture that would give you a
sense for sort of where the electrical potential that all
cells have comes from. You know that cells are bathed
in an extracellular fluid and that that extracellular fluid
contains molecules, including ions or charged
molecules. In fact, the extracellular
fluid is very rich in a particular ion,
sodium, and has lesser amounts of other ions,
potassium and calcium, are the three most important in
the electrical activity of membranes;
sodium, potassium, and calcium. The extracellular space which
is up on the top here is filled with those ions,
in particular, has a high concentration of
sodium. The intracellular space,
or inside the cell, also is a water-rich
environment and also has ions. The ion composition inside the
cell is different than the composition outside the cell in
that the sodium concentration is relatively low.
This chart here shows you for a typical cell sodium
concentration might be 15 mmol while the extracellular sodium
concentration is 145 mmol, so almost ten-fold higher
sodium ion concentration outside the cell than inside the cell.
Well, now you know from what you know about the
structure of lipid membranes that charged molecules,
even though they’re small, charged ions like sodium cannot
penetrate through a lipid bilayer,
so there’s no way for sodium to get through this lipid bilayer.
Even though there’s a very large difference in
concentration, these molecules of sodium on
the outside can’t diffuse inside because they can’t permeate
through the lipid bilayer. Now, potassium,
notice, has a very high concentration inside the cell,
120 mmol, and outside the cell the
concentration is low, 4.5 mmol, so again a big
difference in potassium concentration but going in the
opposite direction. If the membrane was permeable,
sodium would diffuse in and potassium would diffuse out but
it can’t through a plain lipid bilayer.
Well, you also know that cell membranes are not just
lipid bilayers. They have proteins inserted in
them and we talked about proteins that serve as
receptors, for example, the insulin receptor that binds
to insulin. We talked about signal
transduction through those receptors a few weeks ago.
We also talked briefly about the fact that some of these
proteins are transport proteins and their role in the cell
membrane is to allow molecules that the cell needs to come in
or to go out. The glucose transporter is an
example of that. The only way that glucose can
get inside cells to provide a substrate for a metabolism is
because there are specialized proteins in the membrane that
allow glucose to cross, in the same way there are
specialized proteins that allow ions to cross.
These proteins come in two varieties.
Some are active transport proteins like this one which is
called the sodium-potassium pump.
It’s actually a little machine that sits inside the cell
membrane, it’s a protein based machine.
Its job is to pump sodium out of the cell and potassium into
the cell; sodium goes out potassium goes
in. It’s moving those molecules
against their concentration gradients and so energy is
required for that to happen. It doesn’t happen
spontaneously, you can’t move molecules,
molecules don’t spontaneously move from regions of low
concentration to high concentration.
It requires energy and it gets its energy from ATP.
This is called the sodium-potassium pump and it’s
ubiquitous in cells throughout the body.
It’s how cells maintain this low sodium concentration and
high potassium concentration inside.
It’s because they have these little machines in their
membranes that are continually pumping sodium out and potassium
in. Does that make sense?
It’s the action of this pump that causes these differences in
ions to occur. There are other proteins
that serve as channels. You can think of these as very
specialized pores in the membrane that allow ions to pass
through, and they’re selective. This one is a potassium
channel, and so if it is open it allows to potassium to pass
through. It only allows passive
transport. It’s not a machine like the
other one, it’s just a portal or a hole that allows potassium to
move down its concentration gradient.
If this potassium channel is open, then potassium will
naturally move. It will move from high to low
concentration, that is, it’ll move from inside
the cell to out. If sodium–if there’s a channel
for sodium and it happens to be open, and that’s what this is
shown here, a channel with the lid off
means the channel is open, then sodium can pass from its
high concentration to low concentration or from the
extracellular space to the intracellular space.
The cell is in dynamic equilibrium, that in its sort of
steady state, it’s natural state,
there is this active machine that’s pumping sodium out and
potassium in. Then, there are these pores
that when they exist and when they’re open,
are letting these molecules to leak back the other way.
The pump always has to be operating because the leak is
always happening. Does that make sense?
Because you have these differences in ion
concentrations across the cell membrane these–and you have the
flux of molecules continuously across the membrane.
What I’ve shown here are channels that are–they have a
lid on them so they’re sometimes open and sometimes closed,
they can be both opened and closed.
Every cell in your body at a given time is going to have lots
of potassium channels that are open and lots of sodium channels
that are open. They’re just some that are open
all the time. Because of that there’s a
continual leakage of potassium out of the cell and a continual
leakage of sodium into the cell. Well, if ions are moving
across the cell membrane, ions are charged molecules,
and that movement is a current. You usually think of currents
as movements of electrons but movements of ions,
of positively charged ions, is also current.
So, there’s a continual current flow across the membrane.
That continual current flow causes a potential difference
across the membrane. Now, a membrane that’s at rest,
that is in its resting state, is going to have a given number
of channels of sodium and potassium that are open.
So, there’ll be given current of sodium that’s flowing in and
a given current of potassium that’s flowing out.
That’s being compensated by the activity of this pump but this
current flow creates a membrane potential or voltage.
Just like a battery, because these currents are
flowing, if I measure the electrical potential on both
sides of this membrane I would get a voltage difference.
It turns out that for most cells that voltage difference is
negative. The inside of the cell is
slightly negative compared to the outside of the cell and it’s
in the range of -60 to -90 mV. That’s the backdrop,
that’s what you should think of as sort of the resting state of
a membrane, it has these channels in it,
it exists in this fluid environment where there’s high
sodium outside, high potassium inside,
current flows, membrane potential generated.
To make it more complicated there are certain of these ion
channels that exist in open and closed states.
Those open and closed states are regulated by the voltage
across the membrane. Here’s one called the voltage
dependent sodium channel. The resting state,
when the membrane voltage is, let’s say, -90 mV,
the channel is closed, and so this channel does not
allow for sodium to enter. If it opens,
sodium now can enter through new channels.
If there are a lot of these voltage-gated channels on the
surface. They sense a change in voltage,
and they all open, one can have a dramatic change
in the currents that flow through the membrane and hence a
dramatic change in membrane potential.
Now, that’s exactly what happens when we have an action
potential. I show you this diagram that I
showed you a few weeks ago when we were talking about the
nervous system and how it communicates.
I explained it in sort of a superficial way then,
but now you can understand it a little better if you think about
it in terms of these–of the membrane and the membrane having
channels that allow sodium and potassium to flow.
Under a resting condition they have a population of channels
that’s always allowing sodium and potassium to flow,
that creates the potential. Then, they have special
channels that open when the voltage is disturbed in some
way. Here, we’re looking at a
trace of membrane potential in time.
Imagine that you’re very small and you’re sitting on the
surface of this membrane but you have special shoes on that
measure the voltage or something.
You can experience the voltage, the potential drop across the
membrane by just standing on this membrane.
You’re standing there in the resting state,
so you’re watching sodium and potassium go by because of their
normal fluxes, and the potential that you
measure is, say -75 mV. Now, something happens,
there’s some disturbance in the membrane near you,
not right where you’re standing but near you there’s a
disturbance. That disturbance might be a
number of events but what we’ve thought about so far is that
there’s a neurotransmitter that binds.
Somewhere upstream of you there’s a neurotransmitter that
binds to a receptor and it creates a change in membrane
potential. A small change in membrane
potential, but you feel it. When you feel it at your sight
there’s also these voltage sensitive sodium channels that
exist in the membrane around you and they go from the closed
state to the open state. In response to this small
disturbance, some new channels open, these happen to be sodium
channels. They open, a lot of them open
because there’s a lot of them on your cell because your cell is
designed to respond to voltages so it has a lot of these kinds
of channels. Now, what happens when all
these new sodium channels open? There’s a rush of sodium from
outside the cell to inside the cell.
Sodium’s positively charged, you get a rush of current going
by you, and that rush of current depolarizes the membrane.
Remember I said the membrane had a negative potential,
it’s more negative on the inside than outside,
but all of a sudden you’ve opened all these sodium channels
and a rush of sodium goes in, a rush of positively charged
molecules go into the cell, make the inside of the cell
less negative because you’re adding a lot more positive
charge to it. That event is called
depolarization. If you were standing on the
cell with your magic boots that were electrically active somehow
you would experience this dramatic change in membrane
potential. The membrane becoming a lot
less negatively charged, even positively charged.
That’s due totally to this rush of sodium through these new
channels that have opened. Well, there’s a second set
of channels called potassium, voltage-gated potassium
channels that also open but they’re slower than the sodium
channels. When they open they allow a lot
more potassium to rush the other way because, you remember,
potassium is high inside and low outside.
First you get a rush of current going in one direction,
then you get a rush of current going in the other.
What causes in terms of membrane potential is a rapid
depolarization, and then a rapid repolarization
and these channels eventually close again and the membrane
returns to its resting state. If you don’t understand all the
details of that, that’s fine,
it’s described in the book and also described in other membrane
physiology books that you could go to.
It’s not important that you understand all the details but
that you have a sense for what’s happening,
is that within this small region of the cell membrane we
focused on there was some kind of a small disturbance,
it opened all these voltage-gated channels,
caused rushes of current which changed the membrane potential.
That is, in this case what I’ve described to you,
is an action potential. A small change here causes a
large change at my local site, and then I pass that on this
way, because I’m now standing at the
site where there’s a huge disturbance in membrane
potential and that’s going to cause some current to flow,
a little bit to flow downstream. That little bit that flows
downstream is going to cause the voltage-gated channels here to
open, and an action potential to be generated at this site.
If you follow that line of thinking, then an initial
disturbance over here creates a massive membrane potential here,
which moves to here, which moves to here,
which moves to here, and that’s an action potential
being transmitted down a neuron. Make sense?
That’s what we talked about when we were talking about the
nervous system. We were talking about
information flowing from dendrites, dendrites that have
receptors for neurotransmitters, those receptors for
neurotransmitters causing a small membrane disturbance which
then gets converted into an action potential.
That action potential moves down the axon,
say in this direction to that direction. Why doesn’t it move back?
Why does it only move in one direction?
Well, it turns out that it’s very interesting physiology that
when these membrane–when these voltage-gated membrane channels
get opened they become incapable of being reactivated for some
period of time. The voltage-gated sodium
channels open, they close, and then they can’t
be opened again for some period of time.
Just a few milliseconds but long enough for the action
potential to pass out of their region so that you don’t get
currents that flow like–or action potentials that flow like
this. They only flow in one direction
because these channels need to recover.
You understand now a little bit more about why action potentials
flow down axons and when they reach these termini,
the axon termini, what do they do?
This sudden change in membrane potential activates a new
process, and that new process is release of neurotransmitter from
the synapse. That neurotransmitter then
activates another cell, generating an action potential,
sending it down its axon, and so on.
In the nervous system messages pass from
neurotransmitter to action potential, neurotransmitter,
action potential, neurotransmitter,
action potential. Because there might be many,
many neurons impinging on one particular neuron that I’m
interested in and some are sending positive messages,
some are sending negative messages, sending these little
disturbances. Whether this axon generates an
action potential or not depends on the sum total of the small
disturbances that it’s receiving at any one time,
Neurons can integrate information. That information is acquired
from all the neurotransmitters that are impinging on the
dendrites that cause small disturbances that may or may not
add up to the large disturbance which becomes an action
potential. You go on to study neuroscience
or just physiology, you’ll learn more about this
but I think you can probably understand the basic concept.
In the action potential and a neuron we were thinking about a
cell that had a receiving end, that receives neurotransmitter
inputs, that causes membrane potentials to change,
that somehow decides to initiate an action potential.
That action potential flows very rapidly down this
specialized process called an axon,
reaching the axon termini, and then neurotransmitters are
released to the next cell. Heart cells are the same in
that they contain these special voltage-gated membrane channels,
these voltage-gated ion channels that allow for an
action potential to form. They’re capable of doing an
action potential because they have these voltage-gated sodium
and potassium channels. Because of that,
heart muscle cells fall into the same category as nervous–of
neurons in that they’re in the general category called
excitable cells. They’re excitable cells,
means they’re capable of making an action potential.
To have an action potential they need to have these
specialized voltage-gated ion channels in their membranes.
Cardiac myocytes have that, they also have actin and
myosin. They’re muscle cells and
they’re capable of contracting, meaning that this myocyte here
can shorten itself. It can make itself shorter by
contracting just like a muscle, a whole muscle contracts.
That’s different than neurons so they have this
capacity to transmit action potentials;
they have this capacity to contract.
Now, in muscle cells, as we’ll see in a few minutes,
those things are linked. When a muscle cell experiences
an action potential it doesn’t do what a nerve cells does,
which is pass that information along to another cell via
neurotransmitters, instead it contracts.
It also passes along the action potential but it doesn’t do that
through a chemical synapse like in neurons,
it does it through an electrical synapse in that these
cells are very tightly welded together.
Remember we talked about in the nervous system,
the two cells don’t physically touch,
there’s a space in between that’s called the synapse and
it’s over this synapse that neurotransmitters act.
They’re released from the pre-synaptic cell and they
create a change in the post-synaptic cell.
Cardiac myocytes are basically welded together.
In fact, there are special junctions called gap junctions
in between them that allow the easy flow of current.
If an action potential flows through this myocyte,
from this end to the other, it doesn’t have to–it
basically flows straight into the next cell because they’re
directly electrically coupled. If an action potential arises
and comes from this direction, it flows very quickly down this
membrane, it causes this cell to
contract, it flows right into the next cell causing this cell
to contract, flows right into the next cell
causing it to contract. So, in cardiac muscle wherever
the action potential starts it contracts first,
then the action potential flows into the neighboring cells,
they contract. You can think about the cardiac
myocardium, the sheet that I showed you last time,
the muscular walls of the heart, as being sort of a sheet
of these cells that are all connected to each other.
If I start an action potential in one space,
it’s going to flow over the surface.
As it flows over the surface cells will be contracting right
behind it; so electrical flow followed
immediately by contraction locally.
Does that make sense? You could imagine that this
now–because they’re directly electrically coupled,
signals can pass very quickly over the surface of the heart.
They can pass very quickly from one to another,
so I just need to start an action potential in one place,
it’ll be propagated everywhere. I might like to control that
because I’d like to have the heartbeat function in this
controlled fashion we were talking about last time.
So how does the heart solve this problem of control of how
this wave of action potential moves over the surface of the
heart? Well, it does that through a
specialized group of pathways that are collectively called the
cardiac conduction system. This is a terrible diagram.
I’m going to show you the next one, I’ll show you a little bit
better on the next one, and so you’ll see,
it but imagine–just look at the surface here.
This is the heart, the left ventricle,
the left atrium, the right ventricle,
the right atrium, and there’s this pathway.
The heart has something like a nervous system in that this
black region here is a pathway that’s called the cardiac
conduction system. It consists of several
important points. The first is called the
sinoatrial node or SA node and it’s in the right atrium.
The next point is the atrial ventricular node which sits on a
fibrous substance called the septum which separates the atria
from the ventricles. The heart is kind of tilted to
one side, it’s not straight up and down, so the atria are up
here and the ventricles are down here,
there’s a septum in between and that’s where this AV node sits.
It turns out that this septum is electrically
insulating and so if a action potential–a wave of action
potential gets generated up in the atrium,
it stops when it hits the septum, it doesn’t move directly
to the ventricles. The muscles of the atrium and
the muscles of the ventricle are electrically isolated.
The only point of connection between them is this specialized
fiber pathway called the AV node.
That AV node leads into a series of branching fibers that
are called the Purkinje system, Purkinje fibers down here.
These are fibers that very rapidly conduct action
potentials or electrical signals.
What I want you to see in this slide is to notice that while
all of these cells are excitable,
they have the property of generating and sustaining an
action potential, they’re excitable,
an action potential can be generated–the shape of the
action potential varies in different cells.
That’s all this diagram shows you.
You don’t need to know the details but notice that some
things are different. For example,
in the SA node it’s a very slow rise of potential followed by a
slow fall and then a much slower rise again compared to
ventricular muscle, for example,
that has a very rapid uptake, a sustained depolarization
phase and then a rapid repolarization back to baseline.
There are differences in the ways that these things undergo
action potentials. What do you think that’s based
on? What’s different about these
cells? Well, if the action potential
is the result of these voltage-gated channels that must
mean that ventricular muscle cells have a different set of
voltage-gated channels than SA node cells.
They might have totally different molecules that are
doing the transport or they might just have different
numbers of these molecules in their membranes,
but that’s the difference in physiology.
What we’re going to get to the by the end here is I’m going
to try to convince you that this–these changes that are
occurring in individual myocytes,
this rush of current that underlies the action potential
generation is what we measure when we measure an EKG.
That what you’re measuring is sort of the sum of all of these
electrical potentials that are occurring as your heartbeat
changes in electrical–because your heart cells are all
experiencing changes in electrical potential and because
your body is basically a salt solution which conducts
electricity, that you can measure those
changes in electrical potential happening in cells in the heart
by having electrodes just on the surface of your skin.
The EKG arises from all of these action potentials that are
happening within all of the thousands of cells within your
heart. This diagram is a little easier
to understand. It had more words than I liked
so I blocked some of them out. The other one are things that
we’ve already talked about before, the SA node is now
familiar to you, the sinoatrial node,
the AV node, this specialized bundle of His
which carries potential–action potentials very quickly from the
AV node down to the Purkinje system,
and the Purkinje system which branches throughout the
ventricular wall. How does–is a heartbeat
regulated? It turns out that some of these
cells are capable of generating their own action potentials.
They don’t need to be stimulated by some outside
disturbance; they generate an action
potential on their own. The most famous of these is the
SA node up here. The SA node,
if you look at it, here’s the action potential in
the SA node, depolarization, repolarization,
now look what happens here. The cell, when most membranes
we’ve talked about are at resting state,
resting state such that their membrane potential stays
constant until its disturbed by something from outside,
this cell actually is slowly changing its membrane potential
on its own. It does that with a very
consistent frequency, such that at some point this
slow rise of action potential is going–this slow rise of
membrane potential is going to go high enough that it causes
its own disturbance and causes its own action potential.
This is called a self-propagating action
potential. Cells like cells of the SA node
that are capable of doing this have special properties of their
ion channels. The end result is that the SA
node is just making action potentials on a very regular
basis. If you measured,
if you put an electrode, or if you shrunk yourself and
you had your magic boots and you could stand on the SA node,
you would measure an action potential about 60 times a
minute. Once a second,
the SA node is just creating an action potential.
Now, when it creates that action potential what happens?
It disturbs the cells that are around it.
When the SA node creates an action potential it causes a
voltage disturbance in the cells around it and they start making
action potentials. Starting from this source in
the SA node, a wave of action potentials starts to move over
the atrium, over the atria. First the right and then the
left, and what happens as this wave of action potentials
spreads over the atria? What happens–what else do
muscle cells do? They contract,
and so a self-propagating action potential in the SA node
induces an action potential wave that spreads over the atria,
the atria contract. They contract–if you watch
them they contract from the region of the SA node out to the
right slightly before the left, but it passes pretty fast over
these relatively small surface areas.
Now, remember that there’s a septum in between the atrium
and the ventricle so this action potential wave would stop and
not go down to the ventricle except for the AV node.
When the action potential comes down these pathways,
these specialized pathways from the SA node, it reaches the AV
node. The AV node has another special
property in that when it’s stimulated to make an action
potential, it hesitates. It hesitates for a fraction of
a second and then it starts its own action potential.
So, it receives the disturbance, it waits and then
it makes its own action potential.
What happens? Start to put the picture
together now, SA node action potential,
wave of action potential of the atria,
contraction of the atria, AV node gets the signal,
waits, generates an action potential and that action
potential quickly propagates down through the bundle of His
in the Purkinje system. What do they do?
They carry this action potential down into the
ventricles. They start action potentials in
the ventricle, which then passes a wave over
the ventricular muscle, and after that wave of action
potentials comes contraction and ventricular contraction.
Now, why does the AV node wait?
It waits in order to control the heartbeat in the way that we
described last time, so that you want the atria to
contract and deliver their blood to the ventricles before the
ventricle starts to contract. You want the ventricle to wait
until it’s filled up with blood from the atrial contraction and
then start to contract. So, the AV node provides that
separation in time of the atrial contractions and the ventricle
contractions. Now, how would you like the
ventricular–now remember when the ventricle contracts it’s a
big contraction and wants to force blood in what direction?
Up out of the top, that’s where the pulmonary
artery and the aorta are; remember from the model they’re
up at the top of the heart. So, you would like for this
muscle to very effectively eject blood out of the ventricular
chambers and into these two large vessels.
You all have roommates, true;
I don’t know if you all share toothpaste with your roommates,
but if you do then some fraction of you,
probably about half, are irritated with your
roommates because they grab the toothpaste tube at the top.
You might have brothers and sisters who do this,
they grab it near the top and they squeeze it because they
only care about getting their little toothpaste out and so you
get this–that’s not an effective way to get toothpaste
out, squeezing it from the top
because some of the energy goes down into the bottom and forces
this toothpaste down here and the thing gets all out of the
shape. What if you wanted to get all
of the toothpaste out of the tube on one squeeze,
how would you do it? You’d go from the bottom up,
you’d starting squeezing from the bottom and you’d squeeze it
up. If you were good at this,
and you could practice this at home, you get toothpaste and you
could see how much of the–what fraction you can get out with a
single squeeze. I think you’d find your best is
to start from the bottom and squeeze sort of systematically
going up, and that’s what the heart does.
That’s why this Purkinje system is here;
too rapidly conduct signals from the SA node down to the
base of the ventricle and really start the contraction down here.
The contraction starts at the bottom and squeezes up and the
blood is propelled out. One of the roles of the
Purkinje system is to carry this potential into the ventricles in
a way that provides maximum benefit from the contraction of
the cells that result. Now, a couple of other
things that are interesting to know here.
One is that the SA node is not the only collection of cells in
the heart that are capable of generating their own action
potentials. Actually the AV node is also
capable of generating the action potential and so are the cells
in the Purkinje system. They all can generate action
potentials, but it turns out that the SA node does it the
fastest. It does it about 60 beats per
minute. The AV node does it at maybe 40
beats per minute and the Purkinje fibers do it at even a
lower rate than that. What does that mean?
It means that the SA node is functioning properly,
the AV node doesn’t matter what it’s doing in terms of automatic
generation of potentials, because that potential that was
first generated by the SA node arrives at the AV node before it
generates its own potential. Who determines the heart rate?
The fastest beating automatic cell and those are generally in
the SA node. What happens if you have a
disease in your SA node and it stops functioning?
Then the AV node will take over because it’s no longer being
stimulated by the SA nodes action potential and the wave
that results, it will start beating but the
heart will beat slower, it will beat at 40 beats per
minute let’s say. If you had some disease there
and that didn’t work anymore than the Purkinje system–so the
heart has sort of a failsafe system built in such that if
this automatic beat generator fails there are inferior,
not such good quality, but still capable beat
generators further down the line.
Often those–the AV node itself, you’re not going to be
able to function in the same way because you’re not going to get
the same cardiac output because you’re heart isn’t beating fast
enough. There are ways to treat
that now, and the most common way of treating that is by
putting a pacemaker into the heart.
The pacemaker is a device designed by biomedical
engineers, about the size of a hockey puck,
but now even smaller than that, that sits in your chest and it
basically does what the SA node is supposed to do,
generates a potential with a very regular period.
There’s a wire that goes from this artificial device into your
heart, into the atrial muscle, and sits there and stimulates
the tissue around the SA node to replace its function,
so that’s how a pacemaker works. This technology has evolved to
the point where there’s sort of wireless–you can send signals
in, you could change the rate,
you can reprogram the pacemaker without having to take it out
and actually physically reprogram it,
so these are quite sophisticated engineering
devices now. I said something about
action potentials and ion currents.
I’m not going to say anything more about that now.
I will say that in neurons what is important in a propagation of
an action potential is sodium and potassium,
but in muscle cells calcium is also a much more important
player. The reason that calcium is a
much more important player is, as you will learn if you study
more physiology, calcium is the most important
ion in terms of initiating contraction.
So, movement of calcium around muscle cells is very important.
This just shows an action potential in,
for example, a ventricular cell.
It has this rapid upstroke, this plateau in depolarization
and this recovery. So, this might be an action
potential you’d record from a ventricular muscle cell,
and if at the same time you were recording this action
potential and you were also measuring contraction.
Think of this measurement as how much contraction the cell
has done, at this point in its resting state and in this point
it’s in its most contracted state,
then the contraction follows the action potential by about
100 milliseconds. As the contraction happens–as
the action potential happens the contraction happens about
100-150 milliseconds after that, the maximum response;
but these things are coupled but they’re not simultaneous. I think I’ve covered what’s
shown in this slide here. This is just a simpler version
of what we’ve talked about, generation of the signal in the
SA node, movement to the AV node, hesitation.
Then, movement of this signal down the septum in between the
left and the right ventricle, through the Purkinje system,
and the heartbeat being generated in this regular
anatomical pattern. That happens because these
specialized tissues are able to conduct signals very rapidly,
and you can see here in this slide, this is how fast a signal
the velocity of an action potential being propagated
through different tissues goes very rapidly through pathways
like through the atrium, through the bundle of His,
and very rapidly through the Purkinje system.
That’s why the signal gets transmitted so rapidly from the
AV node down to the base of the heart.
These diagrams are in the Power Points which are posted.
I just encourage you to look at them, together with reading the
chapter and hopefully that will help you to understand this
process. Which brings us back to
thinking, at the end, about what I’ve talked about
several times during the lecture;
that is, that you can measure something about the physiology
of the heart by measuring all of this electrical activity.
One way to measure it would be to put electrodes directly into
the heart and physically put them right near the site of
action and measure exactly what’s happening.
That could be–you could get a very detailed picture of what’s
happening in the heart that way. That can be done but that’s an
invasive process. There are cardiologists that do
that, they do this everyday on people.
They put a catheter into your heart, a catheter that goes
through one of the vessels, an artery in your leg.
It’s pushed up into the heart and then there are recording
electrodes on the end and they can measure electrical activity
directly in the heart at different locations.
That’s called cardiac catheterization and cardiac
electrophysiology, and it’s widely used to
diagnose disease in the heart. That’s usually not the
first thing you do because that’s an invasive procedure.
What is important about EKG is that it’s not invasive.
You can do it without entering the body, by just measuring
something that’s happening on the surface.
You can do it very simply by placing electrodes at different
positions on the body. You’ve all seen a diagram like
this that shows a typical trace of an EKG, it’s measured in
milivolt here, it’s a relatively small
potential because there’s some distance–the potentials that
were actually generated in the heart are tens of milivolts,
but you’re measuring at a distance away and so that
signal’s been attenuated, you’re only measuring fractions
of a milivolt at the surface. What you see is a little bump,
followed by a delay, followed by a very big wave,
followed by a delay, followed by one and sometimes
two smaller waves. This is the signal that you
see–that you’ve seen on screens by patients beds in countless
movies and television shows. What do these represent?
Well, they’re called by letters of the alphabet.
This one’s called the P wave that represents the activity
caused during atrial contraction,
so all of those currents that are generated during atrial
contraction show up as a P wave. The QRS complex,
this very big signal here, is contraction of the
ventricle. What does this represent here,
the distance between the P wave and the QRS wave?
This represents the delay in signal transmitting through the
AV node. If your AV node was not
functioning you’d expect that to shorten, that lag would shorten.
You’d also expect that your cardiac performance would not be
so good, because you don’t have this delay then the ventricle is
contracting before it’s fully filled by the atrial
contractions. You can diagnose that
problem, somebody comes in, they’re short of breath,
they’re having trouble, they don’t know what it is,
you measure their EKG, you see that this is shortened
and you know that there’s a problem with their cardiac
conduction system, in particular, with the AV node.
That’s how physicians use these tools.
The T wave is re-polarization of the ventricles.
This is the return of all of this current back into the cell
after this massive depolarization.
The U wave, which is only very rarely seen, represents
relaxation of the muscles, the papillary muscles inside,
which control some of the valve function.
We’ll talk about this more in section.
If you’ve had a full electrocardiogram you’ll know
that they put many electrodes on your body.
They put–a full electrocardiograph would take 12
electrodes and some of them are placed on your limbs and some of
them are placed around your chest,
sort of wrapped around your chest in a fashion.
The reason for doing that is that you can–if you put several
electrodes then you could look at the potential difference
that’s generated by looking at any two of those electrodes.
If I have one up here and one up here and I look at the
voltage difference here, it might not be the same as the
voltage difference measured between here and here.
Why is that? Because your heart is oriented
in space, it’s a three dimensional object.
All of these cells are at particular three-dimensional
positions inside this three dimensional object.
As these currents happen they happen in a very spatially
oriented way. So, the potential difference I
measure at a distance, here and here for example,
is different. It’s sort of like looking
at the heart from different vantage points,
looking at the electrical activity of the heart from
different vantage points. One of the things that
cardiologists have learned how to do is how to look at
potentials that are generated from different spatial
locations, and correlate that with things
that are happening over the complex geography of the heart.
Why do you have more than one electrode?
It’s so you can look at the heart from sort of different
angles. Questions?
Good, see you on Thursday.

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