00:01
Forms of arrhythmia or causes of arrhythmia.
00:03
You can have acquired arrhythmias
which are probably the most common,
or you may have heritable genetic forms.
00:11
Let's deal first with the acquired forms.
00:13
An ischemic injury probably constitutes the
vast majority of acquired arrhythmia propensity.
00:19
So you can have direct damage to any element
of the conduction system from the AV node
all the way down into the Purkinje fibers,
and that may be a source of arrhythmia.
00:31
A damaged SA node will give
you a sick sinus syndrome.
00:35
These patients tend not to be firing at
the sinoatrial node or only intermittently,
so that they don't have the normal kind of
normal heart rates of 60 or 100 beats per minute.
00:46
In fact, because the SA node is not
firing, the AV node says, 'I'll take over'.
00:52
And when the AV no takes over, it has
a much slower depolarization rate.
00:57
And so it has, tends to have a relative
bradycardia, a so-called junctional bradycardia.
01:05
So that's damaged SA node.
01:07
The AV node will take over as the pacemaker,
and you have typically, bradycardia.
01:12
With atrial dilation, and atrial dilation
is the major cause of atrial fibrillation,
you are stretching those internodal fibers, so
they fire either intermittently or fire aberrantly.
01:26
They become irritable, if you will.
01:28
So they can fire sporadically and you can
have completely independent polarizations
since they're not being entrained by
the activity of the sinoatrial node.
01:40
This leads to irregular conduction through
the AV node, as we've already talked about.
01:45
So depending on whether the
signals reaching the AV node arrive
during a a period that will
allow them to be passed through
or whether they arrive in a
relative refractory period,
you may or may not have signal
conduction through the AV node
into the bundle of His, etc.
02:05
So atrial fibrillation will be an irregularly
irregular heartbeat, as we've already talked about.
02:14
We can have direct damage to any
component of the conduction pathway -
AV node, sinoatrial node, the right
and left bundle branches, et cetera.
02:27
Let's look at a normal electrocardiogram.
02:30
And I know elsewhere within the entire
collection of the Lecturio slide sets,
there is a greater and more intense discussion of
what the normal electrocardiogram or ECG looks like
and how to interpret abnormal electrocardiograms.
02:47
For purposes of arrhythmia, though, we're
just going to briefly look at them here.
02:51
So there is a p wave that marches through
that represents atrial contraction,
and we've marked the first three p waves,
little tiny wave, not much myocardium,
and we can see that depolarization.
03:05
And then we have a QRS
ventricular contraction wave.
03:10
So after the atrial contraction, there's
a pause and then the ventricle squeezes.
03:14
Now it's a much bigger spike because there's
more myocardium that's firing all at once.
03:20
That's the QRS ventricular
contraction wave depolarization.
03:24
Then we have a segment called the S to T segment
that is involved with ventricular repolarization.
03:31
So the myocytes are coming back, they
are pumping calcium appropriately
and they're getting ready for the next wave.
03:38
And so there are certain intervals that occur
between the P wave and the QRS complex,
the QRS complex and the T wave.
03:46
And those are going to be important when we're
thinking about certain forms of arrhythmia.
03:52
So the PR interval is
normally 0.12 to 0.20 seconds.
03:57
Depending on disease that may be occurring
in the AV node, that may be longer.
04:02
So you can you can have a prolonged PR interval.
04:06
And sometimes as we'll talk about,
you can have the AV node
so sick or deranged usually due to ischemia
that it kind of intermittently or completely
ignores that signal coming from the atria.
04:20
And then you can have PR intervals
or p waves that kind of march along
totally unlinked to any QRS activity.
04:31
The QRS complex is usually nice and sharp.
04:34
So this is reflecting the rather quick
propagation of signal from the AV node
down through the right and left bundle
branches and into the Purkinje fibers
and then out to the rest of the myocardium.
04:48
The ST segment is indicated 0.05 to 0.15 seconds
and that's our main interval into our T wave,
our repolarization interval.
05:01
Okay, so the dysfunctional AV node will
give us varying degrees of heart block.
05:10
What is being indicated here on the on the
right hand side, you see a little thin fiber,
that's one of the internodal fibers bringing
signal from the sinoatrial node to the AV node.
05:21
In a normal circumstance, it
pauses and then it continues.
05:24
It pauses and then you get a signal propagation
and then you see the QRS complex.
05:30
Okay, now we can have a first degree heart block
where that AV node takes longer to process a signal
and transmit it out through the bundle of His
and into the right and left bundle branches.
05:45
And that prolonged PR interval is
indicative of AV nodal dysfunction.
05:51
By itself, not a huge problem, but it
does portend that you could progress
to second and third degree
heart block, so what are those?
In second degree heart block, the
signal comes in through the AV node
and it is intermittently transmitted.
06:07
So maybe 1 out of 3 times, or 1 out of 2
times that the signal comes into the AV node,
the AV node will pass it along, and at
other times it completely ignores the signal.
06:18
So that is, worsening degree
of AV nodal dysfunction.
06:22
That's kind of a bad thing, and then it
portends getting into third degree heart block,
which is a complete failure
of the signal to propagate.
06:32
The SA is doing its thing, it's sending the signal
along and the AV node is totally blocking it.
06:39
Now the AV node or ventricular myocardium, a
little bit downstream of that, may take over
so they will depolarize at their rate, just not at
the same rate faster rate of the sinoatrial node.
06:51
So you will have a junctional escape rhythm that
happens when there's a third degree heart block,
but it may be at a very, very slow rate.
07:00
It may be 20 or 30 beats per
minute, which may not be sufficient
to provide adequate perfusion
for a particular individual.
07:10
It's also important to note,
once we get the signal out
through the Purkinje fibers
into the individual myocytes,
and then the signal from there is cell
to cell to cell all the way back up.
07:21
And the normal structure and distribution
of gap junctions indicated here
is the little blue rectangles, allows
the movement of calcium currents
from one cell that's been
stimulated into the next cell,
which will bring it to threshold and it
will fire and send calcium to the next cell,
to the next cell, etc. so that we get a nice wave
of contraction through these calcium channels
through the gap junctions that
also allow passage of calcium.
07:47
So that's important.
07:48
If you have unhealthy myocardium, if you
have ischemic cardiomyopathy for example,
then we will tend to get abnormal distribution
and spatial rearrangement of those gap junctions
and you may not get a good, orderly propagation.
08:11
So the cell to cell conduction of a
calcium current through the gap junctions
is also very important for the final step
of getting a coordinated contractile wave
from apex to base in the ventricles.
08:25
So acquired forms of arrhythmia
include ischemia, myocyte hypertrophy.
08:30
Myocyte hypertrophy will make cells much larger.
08:33
We don't change the capillary density,
so the middle of these very large cells
can be relatively ischemic.
08:39
They may lack sufficient ATP
to pump ions appropriately.
08:42
You may have abnormal levels
of calcium or other ions,
and that may cause arrhythmias
in a hypertrophied myocyte.
08:50
Inflammation, such as myocarditis or
sarcoidosis, can also cause arrhythmias.
08:56
In some cases by killing myocytes, but in
other areas by causing areas of fibrosis.
09:03
So all of these changes, ischemia,
myocyte hypertrophy, inflammation
can cause an increased irritability, a
propensity of the individual cardiac myocytes
somewhere along the pathway to
fire when it feels like it aberrantly,
and that can cause arrhythmias.
09:21
So you can get a cell., normally, as the
propagation wave from cell to cell to cell
through the gap junctions progresses as the
cell is brought to threshold and fires,
and then relaxes, there is a period when it
cannot fire again, a relative refractory period.
09:38
If you have increased irritability, it is possible
that we have cells that are returning back
just to a cell as it's coming out of the relative
refractory period and it will fire too soon.
09:53
And then we can develop waves of
aberrant contraction and propagation,
leading to an arrhythmia.
10:00
You can also have non-conducting
material, amyloid or scar fibrosis
from sarcoid or other previous ischemic injury.
10:09
And that will actually also cause the
areas where we can have reentry circuits.
10:13
So if you are a myocyte and then you're connecting
to the next myocyte and then to the next myocyte
and then you encounter scar or you
encounter amyloid, you have to go around
and then you can potentially come
back and develop reentry circuits.
10:28
So those will disrupt the normal signal
propagation cell to cell to cell,
leading to reentry circuits and an arrhythmia.