Arrhythmias are typically treated with either medications
or with electric shock therapy.
Now on the medication side of things
there are different types of medications
that treat arrhythmias,
but before we get into that,
let's quickly review the cardiac action potentials.
So I'm going to draw them out right here.
So we have two different types of action potentials
for cardiac cells.
We have our nodal action potentials
and that means that they work
at the SA and the AV node,
and we also have our non-nodal action potentials.
These work on the non-nodal cells
meaning your cardiac myelocytes.
And I'm going to write that down
because that's an important concept.
So they work on the cardiac myelocytes
as well as the cells that make up the His-Purkinje system.
and cardiac action potentials share
similar characteristics as action potentials
in other parts of the body.
So we have the rapid depolorization phase
in both of these.
We also have the rapid repolarization phase
and it repolarizes down into baseline.
And the change in voltage is due to
different ion channels being opened
during different phases of the action potentials.
So let's talk about the non-nodal action potential first.
What's going on here.
Well we have phase zero.
And phase zero is this rapid depolarization
and this is because we have
an opening of sodium channels.
So sodium channels open,
sodium pours into the cell,
and gives this rapid spike in voltage.
At some point these sodium channels close,
potassium channels open,
so sodium no longer goes into the cell
and as potassium now leaves the cell,
we're going to enter something called phase one,
which again is mediated by potassium channels
and we're going to get this slight dip in voltage
which brings us into phase two.
And in phase two, we have calcium channels that open
while the potassium channels are still open.
So what's going on here?
Calcium is entering the cell as potassium leaves the cell
and the charges sort of balance each other out.
So therefore you get this plateau period
where there's no change in voltage.
Eventually these calcium channels start closing
and you have a lot of open potassium channels
and this brings you to phase three
which is your repolarization phase.
So phase three is this decline in voltage
and is a repolarization phase caused by
a lot of potassium channels being opened
which brings us down to baseline
and that's phase four.
And this is your resting membrane potential
and this is mediated by the cell being
freely permeable or open to potassium.
So that's the action potential for a non-nodal cell,
and again this is the action potential for
a cardiac myelocyte or a cardiac muscle cell.
What about the nodal cells?
Well at first glance you'll notice that the
action potential for the nodal cell
looks a lot different than the non-nodal action potential.
For one thing you don't have phase one or phase two.
All you have is phase zero, phase three,
which is again your repolarization phase,
and phase four.
Now let's talk about what's going on
in this action potential.
So in phase four,
we have this slow rise in voltage
because of open sodium channels.
And at the tail end of the phase four period,
calcium channels start opening.
We hit threshold and a bunch of calcium channels open
and we get this large spike in voltage.
This is phase zero
and again this is because calcium channels are opening.
There's no phase one and phase two.
So we go automatically into phase three
which is this repolarization phase
and this is mediated by
a bunch of opening potassium channels
and eventually we're back down to phase four
where we have the sodium channels again,
opening slowly.
So again, these two action potentials
not only look different
because there's no phase one and phase two
in the nodal action potential,
different ion channels are open during different phases.
Another important piece to point out
is that your area between phase zero and phase three
this is known as your effective refractory period.
It's a window of time when you can't trigger
another phase zero action potential
and I'm going to call it ERP for short.
Again, during your ERP, you can't trigger
another phase zero action potential.
So basically it's like a built-in mechanism
to prevent this all from over firing
and it's kind of like the cell's recovery period.
So what would happen if we increase our ERP?
Well you would increase the amount of time
between depolarizations.
Therefore you'd increase the amount of time
between heartbeats or when this myelocyte can contract
and if you're increasing
the amount of time between heartbeats,
you're decreasing the heart rate.
And I just wanted to point that out,
because that's how some anti-arrhythmics work
and we'll revisit this in a couple seconds.
So we're going to talk about
four different types of anti-arrhythmics
starting with class I,
and these are our sodium channel blockers.
So remember in the non-nodal action potential,
sodium channels are really important
for phase zero.
So if you block sodium channels,
it takes you a longer time to get through phase zero.
So what's happened?
Well before when we had an ERP this long
our ERP is now this long.
We've extended the effective refractory period
and like we said before,
when you extend the effective refractory period,
you're going to have a longer time
between depolarizations,
meaning you have a longer time between heartbeats,
meaning that you're slowing down the heart rate.
And that's why sodium channel blockers
are great for treating supraventricular tachycardias,
which we sometimes call SVTs for short.
Examples of SVTs are atrial fibrillation,
also known as A-fib,
and this is a condition where
the top chambers of the heart are spasming.
You can also use a sodium channel blocker to treat
an SVT caused by Wolff-Parkinson-White syndrome
which causes a certain type of reentrant tachycardia.
And again, these are just
a couple of examples of SVTs
that are treated by sodium channel blockers
So the next class we're going to talk about
are Class II anti-arrhythmics
and these are beta blockers.
Beta blockers work because they decrease
sympathetic stimulation.
They block the beta I receptors
at the SA and the AV node.
I just want to draw out a couple nodal action potentials.
Now how do sympathetics work to increase heart rate?
Well sympathetics work by increasing the slope
of phase IV.
So basically you're hitting thresholds sooner.
And if you hit thresholds sooner,
you're going to have more frequent depolarizations.
Okay, so I'm going to erase this
so we can see how beta blockers work.
Beta blockers work by blocking sympathetics
and if sympathetics increase your phase four slope,
beta blockers are going to work by
decreasing your phase four slope.
So actually it's going to take you longer
to hit threshold.
Once you hit threshold
the action potential will be the same.
But it takes you longer to hit that threshold.
So again, by decreasing the rise of phase four,
you're going to decrease the frequency
of SA node firing
and since beta blockers work at the AV node as well,
you're going to slow conduction through the AV node.
So both of these things are going to work to
decrease heart rate.
And that's why beta blockers are great
at treating SVTs.
Again like A-fib and even atrial flutter.
Beta blockers can also be used for
ventricular tachycardias,
also known as V-tach.
So someone with a history of an SVT or V-tach,
might be put on a beta blocker
to help control their heart rate.
Okay, so the next class we're going to talk about
are class III anti-arrhythmics,
and these are your potassium channel blockers.
These work primarily at non-nodal cells
and where in the non-nodal action potential
is potassium important?
It's important here at phase three.
So when potassium channel blockers are on board,
we're going to get an elongated phase three period
because we're blocking potassium channels.
And what does that do?
Well where we once had an ERP this long,
our effective refractory period is now this long.
Just like with class I drugs,
when we increase our effective refractory period,
there's more time between depolarizations,
meaning there's more time between heart beats,
meaning you are slowing down the heart rate.
And potassium channel blockers are great
for treating SVTs and V-tach.
But something important to note
is that you're phase three of the action potential
corresponds to your QT interval on EKG.
Since potassium channel blockers
elongate your phase three,
you're going to be elongating your QT interval.
And elongating your QT interval is dangerous
because it can lead to a dangerous rhythm called torsades
and this is a type of V-tach.
Torsades is also dangerous because it can disintegrate
into something called ventricular fibrillation.
Also called V-fib.
In V-fib the bottom chambers of the heart are spasming
and nothing is contracting,
so you're not pumping blood to the rest of the body.
That's why V-fib is deadly if it's not treated immediately.
So anyone that has a long QT,
whether it be from medications they're taking
of from a genetic mutation that they're born with,
anyone who has a long QT,
they stay away from potassium channel blockers
because we don't want to throw them into V-fib.
Okay, so let's talk about class IV anti-arrhythmics.
And these are your calcium channel blockers.
Calcium channel blockers come in two types.
You have your dihydropyridine
which is abbreviated DHP for short,
and you have your non-dihydropyridine
calcium channel blockers.
Your non-dihydropyridine calcium channel blockers
work at your SA and your AV nodes.
So they work at the heart.
Where dihydropyridine calcium channel blockers
these work at blood vessels.
Sometimes to remember this
I will erase this O,
and I'll draw in a heart in place of the O,
so that I remember that the
non-dihydropyridine calcium channel blockers
work at the heart.
And again, the dihydropyridine calcium channel blockers
these work at blood vessels.
They have little to no effect at the SA and AV node.
So where in the nodal action potential
are calcium channels important?
Well they're important at phase zero.
So when you have a calcium channel on board,
you're going to hit threshold just as fast,
but it's going to take you longer
to go through your phase zero.
Therefore, you're going to decrease firing
at the SA node,
because it's taking longer to get through phase zero.
So again, because we're decreasing
or delaying the slope
of the phase zero period at the SA node,
we're going to decrease firing of the SA node.
Since they also work at the AV node,
we're going to slow down conduction to the AV node.
and again, both of these will lead to
a slower heart rate.
And since we're slowing heart rate,
calcium channel blockers work great for SVTs.
Now you might be wondering,
why don't they work for tachycardias like V-tach.
Well that's because in studies
they found out that potassium channel blockers
do a better job at treating V-tach
than calcium channel blockers.
So that's why if somebody has V-tach,
they're not going to reach for
a calcium channel blocker first.