Okay. Now this is to our friends the beta
blockers. Look at this.
We got a football player out there.
That's an American football player.
Think of him as like a linebacker blocker.
And so it's labetalol, propranolol,
Those are all some of the olols examples
to help you start to get the idea
that that's one way you can remember
what beta blockers are.
They end in that "olol" ending.
So, how do they work?
Well, beta-adrenergic blockers is
the same thing as a beta blocker.
We're talking about the receptor.
Remember, beta-adrenergic receptors, their job
is to respond to sympathetic
nervous system stimulation.
So, a beta blocker is a medication that fits
into that receptor, but it blocks
that response. So,
if a patient is taking a beta-
adrenergic blocker or
beta blocker, for short,
it's going to prevent the stimulation of
that sympathetic nervous system
and give us the action that we want.
See, it blocks the action of
I know you've heard of these. Like,
epinephrine, think of it like an adrenaline,
norepinephrine is another catecholamine
at these beta-adrenergic receptors.
Because in a healthy body,
here's how it works.
So you're afraid -- something happens.
Your body kicks into high gear.
Your adrenal medulla -- squirts
out these substances.
They race through your body, they
hit the receptors on your heart.
They make it pump harder and faster.
That's what norepinephrine
and epinephrine do.
But if I'm taking a beta blocker,
then I've got a drug that's already comfy,
all cuddled in on that beta receptor.
So, when those catecholamines
get squirted out in my body,
they race all around, but they cannot
bind to the receptors on my heart.
So, therefore, my heart rate is lower,
and it's not pumping as hard.
That's what beta blockers do.
They block that resection.
They are medications
that fit perfectly
onto those beta receptors, and they block
those receptors from being activated.
And receptors that are blocked means
you'll get the opposite response. Now,
in case I didn't make sense,
we'll go into that again. So don't worry.
If it's just starting to settle in in your
brain, I promise you, we'll get there.
See, beta 1 receptor sites are
predominantly in the heart.
Norepinephrine and epinephrine
are the substances that come
out of the adrenal medulla,
and here's what happens when they squirt
out norepinephrine and epinephrine.
The SA node of the heart -- that's the
pacemaker of your heart --
when those beta receptors receive
epinephrine or norepinephrine,
the SA node goes faster.
And the AV node and the Purkinje fibers,
they also increase our conduction velocity.
So, what happens is the SA node's
the pacemaker, goes, SA node,
AV node, Purkinje fibers.
That's how a beat goes through the heart.
When you receive norepinephrine and
epinephrine into those receptors --
it goes through faster. So,
your heart rate is faster,
and the atrial and the ventricular muscles
increase in velocity and conductivity.
Well, those are a lot of words.
All that means is,
your heart is going to be faster and
much stronger and harder,
which is a good thing
because if my sympathetic nervous
system has been stimulated,
I'm likely in danger.
There's a reason my body is perceiving
that I'm going to need to run really fast.
So I'm going to need oxygen,
I'm gonna need that heart pumping fast, and
I'm gonna need lungs that bronchodilate.
Now, bronchodilating is a job
of the beta 2 receptors.
Now, an easy way that I remember this
is that beta 1 receptors are on your
heart, and I have 1 heart.
Beta 2 receptors are on my lungs,
and I have 2 lungs.
So that's how I keep track of where
beta 1 receptors are
and where beta 2 receptors are.
So they get hit with epinephrine from
the adrenal medulla.
And then what happens is
the arterioles dilate in the heart, the
lung, and the skeletal muscle.
Hey, that's cool, because the arterioles
are like the control valves, so
they're going to dilate when those
messengers, epinephrine from
the adrenal medulla,
hits the beta 2 receptors, arterioles dilate.
Now, things are opening wide
up. Those bronchi --
they're dilating because they know
we need more oxygen,
because we're going to need to
run. Think of it as running.
The same response happens when you
get stressed out, emotional, or mad,
but just think of it as if you're going
to need physical ability to run.
Now, the uterus relaxes. That may
seem kind of odd,
that we're talking about it right
here, but let's think about it.
If I was trying to run away from something
that was trying to kill me,
I don't want to drop a baby here.
I also would want to relax my GI tract
because I don't want to
drop anything out here.
So what happens is my gut slows down,
my uterus relaxes so it won't
push out a baby. Now,
what are the odds that this is
going to be happening?
Not really strong, right? That's just
a funny way for you to remember
sympathetic nervous system stimulation.
Arterioles, they dilate.
Bronchi dilate because I need more oxygen.
My uterus relaxes because
I don't want to drop a kid.
And then glycogenolysis in the liver.
See, the body is so amazing.
It picks up that you need more energy, right?
Because if I'm getting to -- trust me. If I'm
going to run, I need a lot more energy.
So, glycogenolysis is your body's
way of breaking out that
stored glycogen into glucose.
So remember, when you have
excess glucose in your blood,
your body takes it in, stores
it in 2 places. Your –
predominantly, your liver and
your skeletal muscle.
When your sympathetic nervous
system is stimulated,
it's amazing that your body knows, "Hey,
break out the stored stuff." Glyco,
right, genolysis, so "lysis," breaking apart.
"Glyco" standing for the sugar,
and "gen," to create.
So that's what glycogenolysis means
and it happens in your liver.
Okay. So you've got a good feel from
this slide. That's a lot of information.
Let's go back over it to make
sure it's solid in your mind.
On 1 side, we have the beta
1 receptor hearts.
On the other -- beta 1 receptor sites.
On the other slide, we have
beta 2 receptor sites.
So make sure you have solid in your mind,
beta 1 receptors are predominantly
on your 1 heart.
Beta 2 receptors are predominantly
in your, what?
Good, bronchi blood vessels
and uterus, which is
not going to apply to a lot, but I want
it to stick in your mind, anyway.
So, when I get the beta-adrenergic
blockers, I'm going to look at
impacting the jobs of these receptors
in your body.
Okay. Now this chart is really
going to be helpful,
so just hang with us as we fill these in.
Now you'll notice it says
"beta 1 receptor sites." Do you see that
on the far side of your screen?
The title of this is "Beta-
block the activation of beta receptors!"
Exclamation point, all right? So
this is to give you context
about what we're talking about.
In 1 column, we're going to talk about
what happens at a beta 1 receptor site
when it receives or it binds to
norepinephrine or epinephrine,
what the response is.
The next column will say
what happens -- uh huh -- if you've given
that patient a beta blocker?
So the drug will beat those guys
to the beta 1 receptor site.
So let's look at that again.
Okay, if a beta 1 receptor site
binds to norepinephrine or epinephrine,
the SA node increases the heart rate.
But if you've given them a beta blocker,
then the heart rate increase is blocked
and the heart rate will, therefore, decrease.
So that's an important point with beta
blockers. Their heart rate will
definitely be lower.
Now, let me tell you why this matters.
Back before I was able to make
some lifestyle changes,
I was on 5 or 6 blood pressure medications.
One of them was a beta blocker.
Beta blockers directly decrease
your heart rate,
so don't ever try to do physical training
with an elevated heart rate when your
patient's on a beta blocker.
So keep that in mind when you're
teaching your patients,
don't do physical activity trying to get
your heart rate to a certain level.
It's going to be a big problem. You'll
do some damage to your heart
before someone on a high-dose beta blocker
can ever get their heart rate
up that high. Why?
Because you've got the beta blocker drug
on the beta 1 receptor,
and the SA node cannot respond to the
increased demand like it normally would
because they're taking a beta blocker.
Now what happens at the AV node
and the Purkinje fibers?
Well, under normal conditions,
when norepinephrine and epinephrine
bind to that beta 1 receptor,
the AV node -- remember that's the pacemaker --
SA node, AV node, Purkinje fibers --
You got all that going on.
AV node and Purkinje fibers, it'll increase
their conduction velocity.
So those fires will --
those impulses will just be tearing through
the heart at a much faster rate,
unless they have a beta blocker on board.
Then that increase in velocity,
that normally happens
when norepinephrine and epinephrine
bind to receptor
So we know their heart rate
will be slower, right,
because the SA node increase is blocked.
The velocity will not be as intense,
so that's another reason why
it won't move through.
Now, again, if we think about
norepinephrine and epinephrine
getting to the beta 1 receptors
on the heart,
the atrial and the ventricular muscle
will increase in velocity and conductivity.
What does that mean?
Atrium, ventricle, atrium, ventricle, atrium,
ventricle are going to be like,
atrium, ventricle, atrium, ventricle,
They're really going to be
a lot more intense,
unless the patient's taking a beta blocker.
So, then, the increase in velocity and
conductivity is blocked. It's not
going as fast and as hard. So you can see,
based on what you already know
about blood pressure,
if the heart rate is slower and
it's not pumping as hard,
my cardiac output is going to be diminished.
Therefore, my blood pressure will be lower.
Okay, so that's pretty cool, right?
That's really what we want.
If we're treating somebody with hypertension,
we really want to go after
the beta 1 receptors.
We would call that medication a selective
or a selective blocker.
It will just impact the beta 1 receptors.
That's usually what we want.
But stop and pause for a minute and think,
"What other beta receptors have we talked
about and where are they located?"
We have beta 1s on your heart,
so where are the other receptors located?
You got it. Beta 2s are located
on your lungs. Good job.
Now, before we leave this chart, make
sure it makes sense to you.
You've got the receptor on 1 side.
What happens in a normal response
when the sympathetic nervous
system is stimulated?
So make sure you've got a note
written to yourself up there
about norepinephrine and
That's the sympathetic nervous
Over the beta blockers, that's what happens
when we give them a med.
Now, let's take a look at our friends,
the beta 2 receptors.
Yep, you just answered that
question about that.
So we're going to look at what
happens when epinephrine
hits the beta 2 receptors, and what happens
if you have a beta blocker
already on the beta 2s.
Now, we talked about selectivity.
Really, what we're looking for is more
of the selective beta blockers
that would just hit the beta 1 receptors.
But in all honesty,
no matter what drug you're on,
if it's a specific cardio selective,
or beta 1 selective beta blocker,
or if you're on one that's non-selective,
it hits both beta 1 and beta 2,
you could still experience
these beta 2 effects,
so keep that in mind when we're talking
about patient education.
So let's look at what epinephrine does.
When it hits the beta 2 receptors,
dilates those arterioles of the heart,
lung, and skeletal muscle.
It's in this diagram too because we're
talking about the lung.
Now, if you've given the patient
a beta blocker,
it's going to block that dilation.
Okay, here's where this becomes
an issue for your patients.
any patient that we send home
on a beta blocker,
we need to make sure that they
understand if they have
any breathing problems,
they need to contact their health
care provider, okay?
So, for you, beta blockers and breathing
problems are bad news.
Beta blockers and breathing problems are bad news.
So, if you're on a non-selective, you're
more likely to have a problem,
but people who are on
a selective one should just
go after cardiac
beta 1 receptors on the heart
still might have this problem.
Sometimes, they're going to need
their lungs to bronchodilate,
and that action will be blocked if
they're taking a beta blocker.
So that's why it's really important
that you teach your patients,
"If you have any breathing problems,
please contact your healthcare provider."
Then they can problem-solve with them
and assign a different type of medication.
Because when it blocks that
dilation of the bronchi,
your patient might feel really
short of breath.
And you don't want that, nor
do any of your patients.
So, you make the difference.
Educate your patients that, "Hey, you
may or may not have this experience.
But if you notice shortness of breath,
you definitely want to do
something about that.
Contact the healthcare provider.
Probably not take your
next beta blocker
based on what the healthcare provider
advises you to do."
Now, the relaxation of the uterus,
this is just kind of a talking
point in here.
Not going to be a major factor when you're
taking beta blockers for hypertension.
We do use beta blockers for
sometimes to maybe
slow down the process of labor,
but that's not the application
we're talking about here.
Now, glycogenolysis in the liver --
breaks down the stored glycogen
when a beta 2 receptor is
hit by epinephrine.
But beta blockers will block this effect.
They will block this genolysis.
This can be particularly problematic
for diabetic patients.
See, a symptom of low blood sugar,
which is the biggest risk for our
patients that are taking insulin.
If someone has low blood sugar,
what happens is the body kicks into the
sympathetic nervous system response.
It tells the liver, "Hey --" When
this epinephrine goes around
and is circulating,
it tells the liver to kick out
stored glycogen to try and
raise that blood sugar.
Here's the problem.
If the patient's taking a beta blocker,
there's 2 things it won't do:
normal signs of low blood sugar,
our fast heart rate,
and their body's going to try and
break out that stored
glycogen into glucose for blood sugar.
But if they have a beta blocker, you're
not going to have that reaction.
So the patient's not going to be able to
respond to a low blood sugar as
quickly and as easily as they
because they're on a beta blocker.
And the other issue is,
you're not going to see the tachycardia. Why?
Because if the patient's taking a
beta blocker -- remember,
you don't get that faster heart rate.
So patients that are diabetic
and taking a beta blocker
won't show you the typical signs
of low blood sugar.
So it's very important that you educate
your patient and their family members
to know that, "Hey, if they start to
kind of show you some confusion,
really check that blood sugar, because you're
not going to see the normal signs of
fast heart rate, and their body is not going
to be able to respond as efficiently
by breaking out stored glycogen."
Now, the last one,
enhanced skeletal muscle contraction,
which everybody wants.
You're not going to have that
on a beta blocker.
So, why does understanding all how receptors
work and their response help you?
Because once you understand
how any receptor
responds when it's activated,
if we're giving any type of histamine,
it's going to be the opposite
of that response.
There's going to be less of that response.
See, this applies to anti-histamines, right?
Instead of allowing histamine
to connect to its receptor,
then that's how anti-histamines work.
Beta blockers are the same thing.
Antagonist, blocker, antis,
that's what all these drugs do, is they
block the response of that receptor.
Now since you know what beta
1s and beta 2s do,
you can easily remember how
the patient will respond.
So the non-selective ones block
both beta 1s and beta 2s.
That's why they're called non-selective.
Labetalol, propranolol, those are
2 really good examples.
Now, the ones that are selective,
these guys are a little newer
and a little more expensive:
atenolol, bisoprolol, esmolol.
Okay. But also keep in mind
that even if it's supposed to be selective,
with certain patients and different times,
they may also have beta 2 stimulated also,
the goal is primarily beta 1,
but it's not exclusively beta 1, depending
on how the patient is doing.
So let's pause for just a minute
and focus on a question.
Let's see if you can remember
some easy things.
Where are beta 1 receptors located?
Good. On the heart.
Where are beta 2 receptors located?
Good. On the lung.
Why do I want a patient with asthma
to be on a selective beta blocker?
Remember the benefit for being
on a selective beta blocker
is we're going to minimize the risk
of that asthma patient
needing to bronchodilate and having
that response blocked.
So we probably would look for another
medication for an asthmatic patient,
but any patient that we put on a beta
blocker, we always teach them,
"Beta blockers and breathing problems
are bad news."