The next topic we're going to cover here
is irregular heartbeats, arrhythmia,
and that can be something
that is just merely annoying,
can cause some morbidity
or can be a cause of death.
So it's a broad spectrum, and there are lots of
kind of interesting little details along the way.
But we're going to cover the big picture
and get into those details as well.
Important to understand the way that the heart
is wired and how we get a conduction wave
that pretty much allows first an atrial
contraction and then a ventricular contraction.
And the ventricular contraction actually has to
start down at the apex, so we squeeze blood up.
Those are kind of the general
To get a contractile wave though, we
need to fire from cell to cell to cell.
And so ultimately, the contractile wave
and the rhythm of that contractile wave
has to happen intrinsically through what's
going on in individual cardiac myocytes.
And there are occasionally some defects
or deficits that can occur in those
that can lead to arrhythmias.
So we're highlighting the
contractile cells of the myocardium.
These represent 99% of the myocardial volume.
As we've discussed previously, it turns
out that they are only about 20 or 25%
of the total number of cells.
There are endothelial cells in the
heart, there are fibroblasts in the heart,
there are the occasional inflammatory cells.
But 99% or so of the myocardial
volume are the contractile cells,
and they're going to be important end stage player
in making sure we get a nice contractile wave.
On the other hand, we have the conduction
fibers and the conduction fibers are in fact,
modified cardiac myocytes.
They are not nerve fibers,
they are not nerve bundles.
They are in fact modified cardiac myocytes, and
they have many of the same structural features.
They actually have sarcomeres, etcetera.
They have a higher glycogen content,
they have some subtle changes,
but they are mainly to conduct signals very rapidly
from one point to another without using nerves.
About 1% of the myocardial volume overall
represents these conduction fibers.
They are going to be important in
initiating the electrical impulse
at the sinoatrial node for the most part, but
if the Sino atrial node doesn't do its thing,
the atrioventricular node has to take over.
They're also going to be important for
the propagation of an electrical impulse.
So it'll start in the sinoatrial
node, go to the atrioventricular node,
quickly get down to the apex all
through these conduction fibers.
At that point, they hand off the signal
to the individual cardiac monocytes,
who will propagate it back
up the rest of the heart.
All right, let's look at the
individual components of this system.
So first of all, is the sinoatrial node.
Sinoatrial node is then going to connect
through kind of ill-defined internodal tracts
that will bring the signal down
to the atrioventricular node.
To entrain the left side of the heart
as well, we have a Bachmann's bundle
that goes out of sinoatrial node and
crosses over into the left atrium.
Okay, now we've got the right and left atrium
beating together, so the atrioventricular node
will hold the signal for just a brief
moment that allows the atrium to contract,
ejecting an additional 10 to 15%
of volume into the left ventricle
before the left ventricle then
contracts to pump blood out.
From the AV node, holding it for just a little
bit, that signal then goes out the bundle of His
and into the right and left bundle
branches and eventually out to ramify
with the individual cardiac myocytes.
The sinoatrialnode is the
natural pacemaker of the heart.
We're just showing you here in
yellow the conduction system
and green highlights where
the sinoatrial node lives.
It has the highest level of automaticity,
meaning that it depolarizes faster,
reaching threshold better than any other
tissue or cell type within the heart.
So it's going to be in control.
The sinoatrial node is also receiving
a lot of input that affect its
natural depolarization tendency.
It's going to have neural input and
it's going to have hormonal input
so we can slow the heart rate
down with the vagus nerve.
We can speed it up with
catecholamines like adrenaline.
So the sinoatrial node is going to
be very sensitive to both of those,
and we will if we look at the sinoatrial
node, also see nerves in close proximity.
It's also got a nice blood vessel supply so that if
we want to bathe it with certain hormones, we can.
The sinoatrial node then tracks down through these
internodal pathways into the atrioventricular node.
And as I've already mentioned,
there's a conduction delay.
This enables an atrial contraction to occur
before the ventricular excitation occurs,
and this again gives us an
additional 10 to 15% atrial kick.
The bundle of His is the only normal connection
between the atria and the ventricles.
It comes off of the atrioventricular
node and then goes, courses down
into the right and left bundle branches.
It's conducting impulses through
those bundle branches and eventually,
spreading out to the ventricular myocardial cells.
The connection at that point
is at the Purkinje fibers.
Again, modified cardiac myocytes.
These are actually recognizable cell types,
but they are kind of at the interface
between the right and left bundle branches
and then the individual cardiac myocytes.
We are then going to spread that
impulse cell to cell to cell to cell,
giving us that ventricular
contraction in a nice wave.
Aberrant rhythms, arrhythmias can be
initiated any part of the conduction system.
It can be at the sinoatriall node, atrioventricula
node, internodal conductions,
Bundle of His, right and left bundle branch.
It can also be at the Purkinje fibers wherever,
and actually also in individual cardiac myocytes.
We'll talk about each of those because they
have slightly different manifestations.