hey everyone it's sarah thread sterner

00:02
sorry and calm and in this video I want
00:04
to be doing an in CLECs review over COPD
00:07
also called chronic obstructive
00:09
pulmonary disease and this video will be
00:12
part one of a two-part series what I'm
00:15
going to be covering is the path of COPD
00:17
the signs and symptoms the different
00:20
types and how it is diagnosed and in
00:23
part two I'm going to be covering the
00:25
medications and the nursing
00:26
interventions so be sure to check out
00:28
that part and as always over here on the
00:31
side or down in the description below
00:32
you can access the quiz and the notes
00:34
that go along with this video so let's
00:37
get started first let's start out
00:38
talking about what is the definition of
00:40
COPD what is this
00:42
it is a pulmonary disease that causes
00:45
chronic obstruction of airflow from the
00:49
lungs so before we get into the
00:51
pathophysiology and dive into this
00:54
lecture let's talk about the key points
00:55
that you need to remember so whenever
00:58
we're talking about the path or the
01:00
signs and symptoms you'll have a little
01:01
basic understanding of what we're
01:03
talking about okay okay so key point one
01:06
with this disease there is limited
01:09
airflow and why is this because the
01:12
bronchioles which you can see right here
01:14
and this right here is a viola sac there
01:17
is inflammation which has become chronic
01:20
and has led to this wrong he'll become
01:22
in deformed and narrow then you have
01:25
excessive mucus production so it's
01:28
limiting the amount of oxygen that can
01:30
get in to the bronchial to go to
01:32
alveolar sac for gas exchange and it's
01:36
limiting the amount of carbon dioxide
01:37
that's coming from the alveolar sac to
01:40
be exhaled so you're going to be getting
01:42
some problems another key point is that
01:44
there is the patient does not have the
01:47
ability to fully exhale and this is due
01:51
to the loss of elasticity in these
01:54
alveolar sacs and here you can see there
01:57
mutated looking in a sense their floppy
02:00
your IV OS X should be nice and circular
02:03
and uniformed and here it's completely
02:06
lost elasticity and what you have Yolo
02:08
sex do is they inflate and deflate
02:11
platon deflate and if they don't have
02:13
their form they fully can't do that and
02:15
if they can't do that you're not going
02:17
to have proper gas exchange so it's
02:19
going to throw your blood Casas off and
02:21
air pockets are going to develop over
02:24
time so we'll talk about that especially
02:26
in your emphysema patients this happens
02:28
okay so COPD is irreversible there's not
02:32
a cure cases vary from patient to
02:35
patient some patients will have a mild
02:37
case while some will have severe I've
02:40
had some patients they cannot talk a
02:42
complete sentence without stopping
02:46
taking breaths or hyperventilating
02:48
during the sentence because they have
02:50
COPD so bad and then some patients I've
02:52
had you wouldn't really know that they
02:54
had COPD unless you sing their test
02:56
results or they told her so it varies
02:57
and COPD is managed with lifestyle
03:01
changes and medications which will
03:03
really go over in part two with the
03:04
nursing interventions patient education
03:06
and the medication regimen now the
03:09
causes of this the most common cause of
03:12
COPD tends to be environmental from
03:16
harmful irritants that the person has
03:18
breathed into their lungs for example
03:20
smoking is a huge cause of this because
03:24
they're smoking their cigarette that all
03:26
those chemicals are constantly entering
03:28
into the lungs exhaling and that wreaks
03:30
havoc on the pulmonary system over time
03:33
however this can happen in people who do
03:36
not smoke for instance say they live in
03:39
an area where there's really bad air
03:41
pollution or their job and they're
03:44
around irritants 24/7 or they're a
03:47
welder maybe don't wear the protective
03:49
mask they need to and they can develop
03:50
this and COPD tends to happen gradually
03:55
people will start to notice signs and
03:57
symptoms in middle age they may start to
04:00
notice that over time they became more
04:03
short of breath with normal activity
04:05
they can normally tolerate they notice
04:07
that they have this chronic sometimes
04:10
productive call constantly especially
04:12
like that smokers Hoff in the morning
04:15
and they're getting real current lung
04:17
infections like pneumonia things like
04:19
that then they go to the doctor the
04:21
doctor runs
04:22
on them and they have this condition now
04:25
let's talk about the types of COPD COPD
04:30
that term is used as a catch-all term
04:32
for diseases that limit airflow so what
04:36
we're going to concentrate in this
04:37
lecture is the one type called chronic
04:40
bronchitis and emphysema so let's talk
04:44
about chronic bronchitis first okay
04:47
sometimes you may hear these patients
04:49
refer to as blue bloaters why are they
04:53
referred to as blue bloaters because
04:55
with emphysema those patients are
04:57
referred to as pink puffers so with the
05:00
blue bloaters with chronic bronchitis
05:02
these patients tend to have cyanosis due
05:05
to the hypoxemia that they're having the
05:08
low oxygen which you will see blue
05:11
around their lips mucous membranes skin
05:13
things like that and they tend to have
05:16
edema swelling in the belly the legs
05:18
because depending on how severe this is
05:22
it leads to right side of heart failure
05:25
so let's look at the path though of
05:27
what's happening with chronic bronchitis
05:29
okay here on this diagram you have what
05:33
a normal healthy lung looks like and
05:35
then over here you have a lung that's
05:37
been affected with COPD specifically we
05:41
have some wrong chronic bronchitis and
05:43
emphysema going on so first let's talk
05:45
live the healthy lung and talk about how
05:47
normally gas exchange goes through this
05:50
and then we'll compare it with a lung
05:52
that's experiencing chronic bronchitis
05:53
so you breathe in some oxygen it goes
05:57
down through your trachea which your
06:00
trachea splits at the chorion up into
06:03
your bronchus your rotten left bronchus
06:05
and rotten lip bronchus your primary
06:07
bronchus enter into the lungs at the
06:08
hilum and then the bronchus even breaks
06:11
and branches off into further smaller
06:13
Airways like your secondary bronchi your
06:16
tertiary bronchi and then eventually
06:18
your bronchioles and then you're a vor
06:20
sacs and yeah and you're a vor sacs are
06:23
opening and closing inflating and
06:26
deflating for gas exchange and what
06:28
helps you to do this breathing is
06:31
whenever you breathe in your diaphragm
06:34
which is normally
06:35
dumb sheep is going to contract and it's
06:37
going to go down and this is going to
06:39
create a negative pressure in your lungs
06:42
to allow you to suck in that air which
06:45
is going to go through gas exchange then
06:47
all that pressure has built up your
06:50
diagram is going to relax back into its
06:53
dome-shaped position that's going from
06:55
all that increased pressure in the lungs
06:57
that's going to cause you to exhale and
06:59
force that air out so they're constantly
07:01
inflating and deflating and you keep a
07:03
nice shape a small hyper-inflated now
07:06
let's look at the COPD lung with chronic
07:09
bronchitis so let's say that this person
07:11
is a smoker and constantly smoking and
07:15
over time the smoke is going through all
07:18
these Airways and just really messing it
07:20
up and as what's happened is that over
07:24
time these little areas you see right
07:26
here your bronchioles have become
07:28
inflamed and they start to produce all
07:32
this mucus so um whenever the person is
07:37
trying to breathe in that oxygen can't
07:40
get to these a viola sacs because all
07:43
these narrow little airways and all this
07:45
mucus in the way so oxygen doesn't get
07:48
in then they're trying to exhale that
07:51
air that they just breathe in well they
07:53
can't exhale it fully because again of
07:57
the narrowing and all that mucus so
07:59
they're going to be retaining the carbon
08:00
dioxide now when that patient takes
08:02
another deep breath in they're going to
08:05
be adding more air volume to whatever
08:08
they already breathe in previously so
08:10
this is going to lead to overtime
08:12
hyperinflation of the lungs lungs going
08:14
to like enlarged
08:15
now when the lung and large is you have
08:17
your diaphragm below your lung it's
08:20
going to cause your diaphragm to flatten
08:23
and whenever it flattens you and have
08:26
issues with being able to breathe
08:28
because your diaphragm does 80% of your
08:30
breathing and then the patient's going
08:32
to start using their accessory muscles
08:33
to breathe which will really see with
08:35
our emphysema patients who are called
08:38
the pink puffers and that's for that
08:39
reason now let's talk a little bit more
08:41
about that gas exchange because
08:44
said there's not enough oxygen getting
08:46
in and we're retaining that carbon
08:48
dioxide so that person's going to be
08:51
experiencing what's called respiratory
08:53
acidosis but because there's not a lot
08:57
of that oxygen getting in because just
09:00
so you go through gas exchange with you
09:02
real fast here's a blown-up version of
09:04
an a vo lie and what happens is that you
09:06
have capillaries on these alveolar sacs
09:09
and this capillary is delivering carbon
09:14
dioxide through this capillary wall to
09:15
be exhaled because that is a waste
09:17
product of metabolism and once they get
09:19
rid of it then these little red blood
09:21
cells want to get re oxygenated because
09:24
right now they're exhausted they've done
09:25
their job through the heart and they
09:27
need more oxygen so oxygen that you've
09:29
breathed in will go through that wall
09:32
and attach to those red blood cells and
09:34
then go back to the heart and become
09:36
through the body and do its job but here
09:39
this is not happening
09:40
so what's going to happen you're going
09:41
to have low amounts of oxygen the
09:44
patient is going to become cyanotic
09:46
we're going to display that cyanosis
09:49
then your body's like wow we've really
09:52
got to compensate for that because if
09:54
you've learned through all of our
09:55
lectures every time something bad
09:57
happens in the body the body tries to do
09:59
something with some other system to help
10:00
compensate it and try to save your life
10:02
so what happens is that the body will
10:05
start increasing the production of these
10:08
red blood cells because it's like well
10:10
if we get some more red blood cells in
10:12
the system we can get the body oxygenate
10:15
because we're not getting a lot of
10:16
oxygen but this causes a problem it
10:18
causes the blood to become too thick
10:21
then the body sees well that's not
10:25
really helping so let's throw some other
10:27
things in so what will happen is that
10:29
there will be an increased pressure in
10:31
the arteries specifically your pulmonary
10:33
artery because remember your pulmonary
10:35
artery brings an oxygenated blood to the
10:40
lungs to become oxygenated then that
10:42
pulmonary vein
10:44
sit back to the left side of the heart
10:47
to be pumped through the body and do its
10:49
job so your pulmonary arteries coming
10:51
from the right side of the heart so what
10:54
happens it starts shifting blood which
10:56
is going to increase the pressure in
10:58
that artery and you're going to get
11:00
what's called pulmonary hypertension and
11:04
whenever you get pulmonary hypertension
11:06
and that artery what is happening is
11:08
that that blood is going to start back
11:11
flowing in that pulmonary artery into
11:14
that right side of the heart and we
11:16
really went in depth in this in a heart
11:18
failure videos and that blood starts
11:21
backing up you start getting a lot of
11:23
problems it will affect your liver
11:25
because you'll get congestion in those
11:26
hepatic veins and fluid will start
11:29
building up in the abdomen eventually
11:31
into the legs and it can even lead to
11:33
left-sided heart failure as well so that
11:36
is where the patient is getting the
11:38
bloating and that's where the blue
11:40
bloating comes from now let's look at
11:42
emphysema these patients are sometimes
11:45
called pink puffers why is that patients
11:50
with emphysema tend not to have the
11:52
cyanosis as with the blue bloaters why
11:55
you get the name pink and the puffers
11:57
comes from what's going on
11:59
due to compensation and because the body
12:02
has low oh two levels from what's going
12:06
on with these alveolar sacs the body
12:08
will hyperventilate increase that
12:10
respiratory rate so in a sense they will
12:12
be puffing in order to breathe they're
12:14
really breathing rapidly to get more
12:17
oxygen in to increase the oxygen level
12:20
so you'll have no sign of cyanosis and
12:23
the pink complexion now let's look at
12:26
what's going on up close
12:28
okay so what's happened is that say for
12:31
instance this patient is a smoker and
12:33
they're inhaling that constant irritant
12:35
to their lungs what happens is that an
12:40
inflammation process starts going on
12:42
because of all that smoke affecting the
12:45
sac and the body actually releases a
12:48
substance that causes those of Yolo sex
12:51
to lose their elasticity so they're not
12:54
going to be inflating and deflating
12:56
properly and they become deformed and
12:58
they don't work and whenever that
13:00
happens it's not good because you're not
13:02
going to have proper gas exchange
13:05
happening where those ovular sacs are
13:09
inflating and deflating which is
13:11
allowing that carbon dioxide to pass
13:14
through that capillary wall so you'll be
13:16
keeping carbon dioxide and it's not
13:18
going to allow that oxygen to attach to
13:20
those red blood cells to go through the
13:22
body so you're going to have low oxygen
13:24
now also another thing that happens
13:27
because you're those sacs are not fully
13:30
deflating because they don't work good
13:32
air is going to get trapped in those
13:35
sacks which is going to lead to
13:38
hyperinflation of the lungs and whenever
13:41
the lungs enlarge remember what's below
13:43
your lungs is your diaphragm and the
13:46
diaphragm is going to go from that
13:47
beautiful dome shape to flatten and how
13:50
you the way you breathe what makes it
13:54
effortlessly is your diaphragm it plays
13:57
a huge role in it so to compensate
14:00
because the lungs have to in a sense
14:03
squeeze that air out the body is going
14:06
to start using accessory muscles on your
14:09
chest to help the person get that air
14:13
out and they're also going to
14:16
hyperventilate to get that air out and
14:18
to hopefully get some more oxygen in so
14:22
this will lead because they're using
14:25
their accessory muscles so much to that
14:27
barrel chest look that patients with a
14:30
massima may have which is that increase
14:33
anterior posterior diameter that you may
14:35
see on inspection and the
14:39
hyperventilation again is the
14:41
compensation to help get that oxygen
14:44
level where it needs to be so that's why
14:46
you're not going to see
14:48
we're not going to be blue while they'll
14:50
have that pink complexion compared to
14:53
patients who have chronic bronchitis now
14:56
let's talk about the signs and symptoms
14:57
of COPD to help you remember the typical
15:00
signs and symptoms of COPD let's
15:03
remember the mnemonic lung damage
15:05
because that is what is going on with
15:07
COPD they have lung damage to the lungs
15:10
that is limiting the airflow from the
15:13
lung so el they are going to have lack
15:17
of energy and this is because they have
15:19
a limited supply of oxygen flooding
15:22
through the body in order for your
15:23
organs and everything to work properly
15:25
it needs oxygen so anything for them
15:28
for them to do is very hard and requires
15:30
a lot of effort you for unable to
15:33
tolerate activity they will get a lot of
15:36
short really short of breath and if they
15:38
have it really severe even getting them
15:39
from a chair to the back to the bed or
15:42
walking to the bathroom it's a big deal
15:44
and it makes them very short of breath
15:46
in for nutrition it will be poor
15:50
especially with your patients within
15:52
fuzzy manaos link back to the path oh
15:55
why would they have poor nutrition well
15:57
they are spending a lot of energy
16:01
breathing and they're burning more
16:03
calories than normal a person with
16:05
healthy lungs would burn just with their
16:08
breathing so they're going to have
16:09
weight loss also eating if they have it
16:12
really released severe and just chewing
16:16
their food and swallowing their food
16:18
exhausts them so they may not be up to
16:21
eating so you really have to manage that
16:23
which we'll talk about nursing
16:24
interventions with your patients with
16:26
emphysema g4 gases abnormal those
16:30
arterial gases your po2 pco2 will be
16:34
greater than 45 usually that's carbon
16:37
dioxide and your po2 which measures your
16:40
oxygen less than 90 because remember
16:42
they have low oxygen and high carbon
16:44
dioxide and usually we'll have
16:47
respiratory acidosis because of those
16:49
lab results D for dry or productive call
16:53
and the productive cough all these
16:55
possible be constant and chronic
16:58
patients will call it wrong card
16:59
tend to have the productive cough
17:01
because remember they have the increased
17:03
mucus production from where those
17:05
bronchioles have become flamed and they
17:08
narrowed so that's why they have that a
17:10
four accessory muscle usage for
17:13
breathing again that was with your
17:15
patients with emphysema and that was
17:17
because that diaphragm has flattened
17:20
those lungs are hyper-inflated so now
17:23
they their diaphragms aren't there to
17:25
help them exhale that air so they've got
17:28
to compensate by using those accessory
17:29
muscles and the other a for abnormal
17:33
lung sounds
17:34
it can vary they can be diminished where
17:36
you don't hear much of anything
17:38
especially in those lower bases coarse
17:41
crackles especially in your chronic
17:44
bronchitis because of that you because
17:46
that's what you're going to be hearing
17:47
or wheezing and I have a whole video if
17:49
you're not familiar with what these lung
17:51
sounds sound like a card should be
17:52
popping up and you can access the video
17:55
it has audio clips where you can
17:56
actually hear these lung sounds in for
17:59
modification of skin color from pink to
18:02
cyanosis and this again was with her
18:05
chronic bronchitis patients they have a
18:09
tendency because of their low oxygen
18:11
will have the blue around lips or mucous
18:14
membranes or the skin and a four
18:17
anterior-posterior diameter increase and
18:20
that's that barrel chest look and that's
18:22
mainly with the patients who are
18:23
suffering from emphysema because the
18:25
usage of those accessory muscles built
18:28
up the chest and the hyperinflation of
18:30
the lungs G and four gets in the tripod
18:34
position to breathe a lot of times in
18:37
order to help these patients breathe
18:39
whenever they're having difficulty
18:41
breathing they will get in the tripod
18:42
position and this is where they're
18:45
standing they're leaning forward and
18:48
while supporting their hands on their
18:50
knees or on an object and just being
18:52
bent over like that helps them breathe
18:55
better so you may see that sometimes and
18:57
ii4 extreme disney a-- and that just
19:00
goes along with everything that's going
19:02
on they just get really short of breath
19:03
a lot of times now let's look at the
19:06
complications of COPD and how it is
19:09
diagnosed
19:11
and a few complications a patient could
19:13
experience with COPD is heart disease
19:16
like heart failure again and we talked
19:20
about that with the path especially the
19:21
chronic bronchitis patients it can lead
19:24
to pulmonary hypertension which will
19:27
cause increased pressure on that right
19:30
side of that ventricle and I mean get
19:32
right-sided heart failure
19:33
another thing is pneumothorax where the
19:36
lung just collapses spontaneously
19:39
and this tends to be spontaneous and
19:41
patients who have a history of COPD and
19:44
it's because of the formation of those
19:46
air sacs in those alveoli and especially
19:49
your patients with emphysema and I have
19:51
had patients who have been admitted with
19:53
this so this does happen I have seen it
19:55
lung infections pneumonia for instance
19:59
and they have an increased risk of
20:01
developing lung cancer okay so how is
20:04
this diagnosed from a nursing standpoint
20:06
just be familiar with what may be
20:08
ordered so if you're taking care of a
20:10
patient with this you know what to look
20:12
for for their test results and
20:14
physicians will order what's called a
20:16
spirometry which is a test where
20:19
patients breathe into a tube which
20:22
measures the following it's going to
20:25
measure how much volume the lungs can
20:27
hold during inhalation and it's going to
20:30
measure how much and how fast air volume
20:33
is being exhaled because remember that's
20:35
the whole problem with this disease
20:37
process they have an issue with
20:39
retaining too much so they don't exhale
20:41
too much compared to how much they took
20:43
in so it will measure that and what it's
20:45
measuring the two things mainly is it's
20:49
measuring the the fvc which is the
20:52
forced vital capacity and if they get a
20:55
low reading on this this represents
20:57
restrictive breathing and this is the
20:59
largest amount of air exhaled after
21:02
breathing in deeply in one second
21:05
another thing it looks at is it measures
21:08
the force expert ory
21:10
volume which is how much air a person
21:13
can exhale within one second and a low
21:17
reading will end
21:19
okay how severe the disease process
21:21
actually is so that is about COPD part
21:25
one now be sure to check out part two
21:27
and don't forget to take the in CLECs
21:28
review quiz that goes along with this
21:31
lecture and thank you so much for
21:32
watching and please consider subscribing
21:33
to this YouTube channel
hey everyone it's sarah thread sterner
00:02
sorry and calm and in this video I want
00:04
to be doing an in CLECs review over COPD
00:07
also called chronic obstructive
00:09
pulmonary disease and this video will be
00:12
part one of a two-part series what I'm
00:15
going to be covering is the path of COPD
00:17
the signs and symptoms the different
00:20
types and how it is diagnosed and in
00:23
part two I'm going to be covering the
00:25
medications and the nursing
00:26
interventions so be sure to check out
00:28
that part and as always over here on the
00:31
side or down in the description below
00:32
you can access the quiz and the notes
00:34
that go along with this video so let's
00:37
get started first let's start out
00:38
talking about what is the definition of
00:40
COPD what is this
00:42
it is a pulmonary disease that causes
00:45
chronic obstruction of airflow from the
00:49
lungs so before we get into the
00:51
pathophysiology and dive into this
00:54
lecture let's talk about the key points
00:55
that you need to remember so whenever
00:58
we're talking about the path or the
01:00
signs and symptoms you'll have a little
01:01
basic understanding of what we're
01:03
talking about okay okay so key point one
01:06
with this disease there is limited
01:09
airflow and why is this because the
01:12
bronchioles which you can see right here
01:14
and this right here is a viola sac there
01:17
is inflammation which has become chronic
01:20
and has led to this wrong he'll become
01:22
in deformed and narrow then you have
01:25
excessive mucus production so it's
01:28
limiting the amount of oxygen that can
01:30
get in to the bronchial to go to
01:32
alveolar sac for gas exchange and it's
01:36
limiting the amount of carbon dioxide
01:37
that's coming from the alveolar sac to
01:40
be exhaled so you're going to be getting
01:42
some problems another key point is that
01:44
there is the patient does not have the
01:47
ability to fully exhale and this is due
01:51
to the loss of elasticity in these
01:54
alveolar sacs and here you can see there
01:57
mutated looking in a sense their floppy
02:00
your IV OS X should be nice and circular
02:03
and uniformed and here it's completely
02:06
lost elasticity and what you have Yolo
02:08
sex do is they inflate and deflate
02:11
platon deflate and if they don't have
02:13
their form they fully can't do that and
02:15
if they can't do that you're not going
02:17
to have proper gas exchange so it's
02:19
going to throw your blood Casas off and
02:21
air pockets are going to develop over
02:24
time so we'll talk about that especially
02:26
in your emphysema patients this happens
02:28
okay so COPD is irreversible there's not
02:32
a cure cases vary from patient to
02:35
patient some patients will have a mild
02:37
case while some will have severe I've
02:40
had some patients they cannot talk a
02:42
complete sentence without stopping
02:46
taking breaths or hyperventilating
02:48
during the sentence because they have
02:50
COPD so bad and then some patients I've
02:52
had you wouldn't really know that they
02:54
had COPD unless you sing their test
02:56
results or they told her so it varies
02:57
and COPD is managed with lifestyle
03:01
changes and medications which will
03:03
really go over in part two with the
03:04
nursing interventions patient education
03:06
and the medication regimen now the
03:09
causes of this the most common cause of
03:12
COPD tends to be environmental from
03:16
harmful irritants that the person has
03:18
breathed into their lungs for example
03:20
smoking is a huge cause of this because
03:24
they're smoking their cigarette that all
03:26
those chemicals are constantly entering
03:28
into the lungs exhaling and that wreaks
03:30
havoc on the pulmonary system over time
03:33
however this can happen in people who do
03:36
not smoke for instance say they live in
03:39
an area where there's really bad air
03:41
pollution or their job and they're
03:44
around irritants 24/7 or they're a
03:47
welder maybe don't wear the protective
03:49
mask they need to and they can develop
03:50
this and COPD tends to happen gradually
03:55
people will start to notice signs and
03:57
symptoms in middle age they may start to
04:00
notice that over time they became more
04:03
short of breath with normal activity
04:05
they can normally tolerate they notice
04:07
that they have this chronic sometimes
04:10
productive call constantly especially
04:12
like that smokers Hoff in the morning
04:15
and they're getting real current lung
04:17
infections like pneumonia things like
04:19
that then they go to the doctor the
04:21
doctor runs
04:22
on them and they have this condition now
04:25
let's talk about the types of COPD COPD
04:30
that term is used as a catch-all term
04:32
for diseases that limit airflow so what
04:36
we're going to concentrate in this
04:37
lecture is the one type called chronic
04:40
bronchitis and emphysema so let's talk
04:44
about chronic bronchitis first okay
04:47
sometimes you may hear these patients
04:49
refer to as blue bloaters why are they
04:53
referred to as blue bloaters because
04:55
with emphysema those patients are
04:57
referred to as pink puffers so with the
05:00
blue bloaters with chronic bronchitis
05:02
these patients tend to have cyanosis due
05:05
to the hypoxemia that they're having the
05:08
low oxygen which you will see blue
05:11
around their lips mucous membranes skin
05:13
things like that and they tend to have
05:16
edema swelling in the belly the legs
05:18
because depending on how severe this is
05:22
it leads to right side of heart failure
05:25
so let's look at the path though of
05:27
what's happening with chronic bronchitis
05:29
okay here on this diagram you have what
05:33
a normal healthy lung looks like and
05:35
then over here you have a lung that's
05:37
been affected with COPD specifically we
05:41
have some wrong chronic bronchitis and
05:43
emphysema going on so first let's talk
05:45
live the healthy lung and talk about how
05:47
normally gas exchange goes through this
05:50
and then we'll compare it with a lung
05:52
that's experiencing chronic bronchitis
05:53
so you breathe in some oxygen it goes
05:57
down through your trachea which your
06:00
trachea splits at the chorion up into
06:03
your bronchus your rotten left bronchus
06:05
and rotten lip bronchus your primary
06:07
bronchus enter into the lungs at the
06:08
hilum and then the bronchus even breaks
06:11
and branches off into further smaller
06:13
Airways like your secondary bronchi your
06:16
tertiary bronchi and then eventually
06:18
your bronchioles and then you're a vor
06:20
sacs and yeah and you're a vor sacs are
06:23
opening and closing inflating and
06:26
deflating for gas exchange and what
06:28
helps you to do this breathing is
06:31
whenever you breathe in your diaphragm
06:34
which is normally
06:35
dumb sheep is going to contract and it's
06:37
going to go down and this is going to
06:39
create a negative pressure in your lungs
06:42
to allow you to suck in that air which
06:45
is going to go through gas exchange then
06:47
all that pressure has built up your
06:50
diagram is going to relax back into its
06:53
dome-shaped position that's going from
06:55
all that increased pressure in the lungs
06:57
that's going to cause you to exhale and
06:59
force that air out so they're constantly
07:01
inflating and deflating and you keep a
07:03
nice shape a small hyper-inflated now
07:06
let's look at the COPD lung with chronic
07:09
bronchitis so let's say that this person
07:11
is a smoker and constantly smoking and
07:15
over time the smoke is going through all
07:18
these Airways and just really messing it
07:20
up and as what's happened is that over
07:24
time these little areas you see right
07:26
here your bronchioles have become
07:28
inflamed and they start to produce all
07:32
this mucus so um whenever the person is
07:37
trying to breathe in that oxygen can't
07:40
get to these a viola sacs because all
07:43
these narrow little airways and all this
07:45
mucus in the way so oxygen doesn't get
07:48
in then they're trying to exhale that
07:51
air that they just breathe in well they
07:53
can't exhale it fully because again of
07:57
the narrowing and all that mucus so
07:59
they're going to be retaining the carbon
08:00
dioxide now when that patient takes
08:02
another deep breath in they're going to
08:05
be adding more air volume to whatever
08:08
they already breathe in previously so
08:10
this is going to lead to overtime
08:12
hyperinflation of the lungs lungs going
08:14
to like enlarged
08:15
now when the lung and large is you have
08:17
your diaphragm below your lung it's
08:20
going to cause your diaphragm to flatten
08:23
and whenever it flattens you and have
08:26
issues with being able to breathe
08:28
because your diaphragm does 80% of your
08:30
breathing and then the patient's going
08:32
to start using their accessory muscles
08:33
to breathe which will really see with
08:35
our emphysema patients who are called
08:38
the pink puffers and that's for that
08:39
reason now let's talk a little bit more
08:41
about that gas exchange because
08:44
said there's not enough oxygen getting
08:46
in and we're retaining that carbon
08:48
dioxide so that person's going to be
08:51
experiencing what's called respiratory
08:53
acidosis but because there's not a lot
08:57
of that oxygen getting in because just
09:00
so you go through gas exchange with you
09:02
real fast here's a blown-up version of
09:04
an a vo lie and what happens is that you
09:06
have capillaries on these alveolar sacs
09:09
and this capillary is delivering carbon
09:14
dioxide through this capillary wall to
09:15
be exhaled because that is a waste
09:17
product of metabolism and once they get
09:19
rid of it then these little red blood
09:21
cells want to get re oxygenated because
09:24
right now they're exhausted they've done
09:25
their job through the heart and they
09:27
need more oxygen so oxygen that you've
09:29
breathed in will go through that wall
09:32
and attach to those red blood cells and
09:34
then go back to the heart and become
09:36
through the body and do its job but here
09:39
this is not happening
09:40
so what's going to happen you're going
09:41
to have low amounts of oxygen the
09:44
patient is going to become cyanotic
09:46
we're going to display that cyanosis
09:49
then your body's like wow we've really
09:52
got to compensate for that because if
09:54
you've learned through all of our
09:55
lectures every time something bad
09:57
happens in the body the body tries to do
09:59
something with some other system to help
10:00
compensate it and try to save your life
10:02
so what happens is that the body will
10:05
start increasing the production of these
10:08
red blood cells because it's like well
10:10
if we get some more red blood cells in
10:12
the system we can get the body oxygenate
10:15
because we're not getting a lot of
10:16
oxygen but this causes a problem it
10:18
causes the blood to become too thick
10:21
then the body sees well that's not
10:25
really helping so let's throw some other
10:27
things in so what will happen is that
10:29
there will be an increased pressure in
10:31
the arteries specifically your pulmonary
10:33
artery because remember your pulmonary
10:35
artery brings an oxygenated blood to the
10:40
lungs to become oxygenated then that
10:42
pulmonary vein
10:44
sit back to the left side of the heart
10:47
to be pumped through the body and do its
10:49
job so your pulmonary arteries coming
10:51
from the right side of the heart so what
10:54
happens it starts shifting blood which
10:56
is going to increase the pressure in
10:58
that artery and you're going to get
11:00
what's called pulmonary hypertension and
11:04
whenever you get pulmonary hypertension
11:06
and that artery what is happening is
11:08
that that blood is going to start back
11:11
flowing in that pulmonary artery into
11:14
that right side of the heart and we
11:16
really went in depth in this in a heart
11:18
failure videos and that blood starts
11:21
backing up you start getting a lot of
11:23
problems it will affect your liver
11:25
because you'll get congestion in those
11:26
hepatic veins and fluid will start
11:29
building up in the abdomen eventually
11:31
into the legs and it can even lead to
11:33
left-sided heart failure as well so that
11:36
is where the patient is getting the
11:38
bloating and that's where the blue
11:40
bloating comes from now let's look at
11:42
emphysema these patients are sometimes
11:45
called pink puffers why is that patients
11:50
with emphysema tend not to have the
11:52
cyanosis as with the blue bloaters why
11:55
you get the name pink and the puffers
11:57
comes from what's going on
11:59
due to compensation and because the body
12:02
has low oh two levels from what's going
12:06
on with these alveolar sacs the body
12:08
will hyperventilate increase that
12:10
respiratory rate so in a sense they will
12:12
be puffing in order to breathe they're
12:14
really breathing rapidly to get more
12:17
oxygen in to increase the oxygen level
12:20
so you'll have no sign of cyanosis and
12:23
the pink complexion now let's look at
12:26
what's going on up close
12:28
okay so what's happened is that say for
12:31
instance this patient is a smoker and
12:33
they're inhaling that constant irritant
12:35
to their lungs what happens is that an
12:40
inflammation process starts going on
12:42
because of all that smoke affecting the
12:45
sac and the body actually releases a
12:48
substance that causes those of Yolo sex
12:51
to lose their elasticity so they're not
12:54
going to be inflating and deflating
12:56
properly and they become deformed and
12:58
they don't work and whenever that
13:00
happens it's not good because you're not
13:02
going to have proper gas exchange
13:05
happening where those ovular sacs are
13:09
inflating and deflating which is
13:11
allowing that carbon dioxide to pass
13:14
through that capillary wall so you'll be
13:16
keeping carbon dioxide and it's not
13:18
going to allow that oxygen to attach to
13:20
those red blood cells to go through the
13:22
body so you're going to have low oxygen
13:24
now also another thing that happens
13:27
because you're those sacs are not fully
13:30
deflating because they don't work good
13:32
air is going to get trapped in those
13:35
sacks which is going to lead to
13:38
hyperinflation of the lungs and whenever
13:41
the lungs enlarge remember what's below
13:43
your lungs is your diaphragm and the
13:46
diaphragm is going to go from that
13:47
beautiful dome shape to flatten and how
13:50
you the way you breathe what makes it
13:54
effortlessly is your diaphragm it plays
13:57
a huge role in it so to compensate
14:00
because the lungs have to in a sense
14:03
squeeze that air out the body is going
14:06
to start using accessory muscles on your
14:09
chest to help the person get that air
14:13
out and they're also going to
14:16
hyperventilate to get that air out and
14:18
to hopefully get some more oxygen in so
14:22
this will lead because they're using
14:25
their accessory muscles so much to that
14:27
barrel chest look that patients with a
14:30
massima may have which is that increase
14:33
anterior posterior diameter that you may
14:35
see on inspection and the
14:39
hyperventilation again is the
14:41
compensation to help get that oxygen
14:44
level where it needs to be so that's why
14:46
you're not going to see
14:48
we're not going to be blue while they'll
14:50
have that pink complexion compared to
14:53
patients who have chronic bronchitis now
14:56
let's talk about the signs and symptoms
14:57
of COPD to help you remember the typical
15:00
signs and symptoms of COPD let's
15:03
remember the mnemonic lung damage
15:05
because that is what is going on with
15:07
COPD they have lung damage to the lungs
15:10
that is limiting the airflow from the
15:13
lung so el they are going to have lack
15:17
of energy and this is because they have
15:19
a limited supply of oxygen flooding
15:22
through the body in order for your
15:23
organs and everything to work properly
15:25
it needs oxygen so anything for them
15:28
for them to do is very hard and requires
15:30
a lot of effort you for unable to
15:33
tolerate activity they will get a lot of
15:36
short really short of breath and if they
15:38
have it really severe even getting them
15:39
from a chair to the back to the bed or
15:42
walking to the bathroom it's a big deal
15:44
and it makes them very short of breath
15:46
in for nutrition it will be poor
15:50
especially with your patients within
15:52
fuzzy manaos link back to the path oh
15:55
why would they have poor nutrition well
15:57
they are spending a lot of energy
16:01
breathing and they're burning more
16:03
calories than normal a person with
16:05
healthy lungs would burn just with their
16:08
breathing so they're going to have
16:09
weight loss also eating if they have it
16:12
really released severe and just chewing
16:16
their food and swallowing their food
16:18
exhausts them so they may not be up to
16:21
eating so you really have to manage that
16:23
which we'll talk about nursing
16:24
interventions with your patients with
16:26
emphysema g4 gases abnormal those
16:30
arterial gases your po2 pco2 will be
16:34
greater than 45 usually that's carbon
16:37
dioxide and your po2 which measures your
16:40
oxygen less than 90 because remember
16:42
they have low oxygen and high carbon
16:44
dioxide and usually we'll have
16:47
respiratory acidosis because of those
16:49
lab results D for dry or productive call
16:53
and the productive cough all these
16:55
possible be constant and chronic
16:58
patients will call it wrong card
16:59
tend to have the productive cough
17:01
because remember they have the increased
17:03
mucus production from where those
17:05
bronchioles have become flamed and they
17:08
narrowed so that's why they have that a
17:10
four accessory muscle usage for
17:13
breathing again that was with your
17:15
patients with emphysema and that was
17:17
because that diaphragm has flattened
17:20
those lungs are hyper-inflated so now
17:23
they their diaphragms aren't there to
17:25
help them exhale that air so they've got
17:28
to compensate by using those accessory
17:29
muscles and the other a for abnormal
17:33
lung sounds
17:34
it can vary they can be diminished where
17:36
you don't hear much of anything
17:38
especially in those lower bases coarse
17:41
crackles especially in your chronic
17:44
bronchitis because of that you because
17:46
that's what you're going to be hearing
17:47
or wheezing and I have a whole video if
17:49
you're not familiar with what these lung
17:51
sounds sound like a card should be
17:52
popping up and you can access the video
17:55
it has audio clips where you can
17:56
actually hear these lung sounds in for
17:59
modification of skin color from pink to
18:02
cyanosis and this again was with her
18:05
chronic bronchitis patients they have a
18:09
tendency because of their low oxygen
18:11
will have the blue around lips or mucous
18:14
membranes or the skin and a four
18:17
anterior-posterior diameter increase and
18:20
that's that barrel chest look and that's
18:22
mainly with the patients who are
18:23
suffering from emphysema because the
18:25
usage of those accessory muscles built
18:28
up the chest and the hyperinflation of
18:30
the lungs G and four gets in the tripod
18:34
position to breathe a lot of times in
18:37
order to help these patients breathe
18:39
whenever they're having difficulty
18:41
breathing they will get in the tripod
18:42
position and this is where they're
18:45
standing they're leaning forward and
18:48
while supporting their hands on their
18:50
knees or on an object and just being
18:52
bent over like that helps them breathe
18:55
better so you may see that sometimes and
18:57
ii4 extreme disney a-- and that just
19:00
goes along with everything that's going
19:02
on they just get really short of breath
19:03
a lot of times now let's look at the
19:06
complications of COPD and how it is
19:09
diagnosed
19:11
and a few complications a patient could
19:13
experience with COPD is heart disease
19:16
like heart failure again and we talked
19:20
about that with the path especially the
19:21
chronic bronchitis patients it can lead
19:24
to pulmonary hypertension which will
19:27
cause increased pressure on that right
19:30
side of that ventricle and I mean get
19:32
right-sided heart failure
19:33
another thing is pneumothorax where the
19:36
lung just collapses spontaneously
19:39
and this tends to be spontaneous and
19:41
patients who have a history of COPD and
19:44
it's because of the formation of those
19:46
air sacs in those alveoli and especially
19:49
your patients with emphysema and I have
19:51
had patients who have been admitted with
19:53
this so this does happen I have seen it
19:55
lung infections pneumonia for instance
19:59
and they have an increased risk of
20:01
developing lung cancer okay so how is
20:04
this diagnosed from a nursing standpoint
20:06
just be familiar with what may be
20:08
ordered so if you're taking care of a
20:10
patient with this you know what to look
20:12
for for their test results and
20:14
physicians will order what's called a
20:16
spirometry which is a test where
20:19
patients breathe into a tube which
20:22
measures the following it's going to
20:25
measure how much volume the lungs can
20:27
hold during inhalation and it's going to
20:30
measure how much and how fast air volume
20:33
is being exhaled because remember that's
20:35
the whole problem with this disease
20:37
process they have an issue with
20:39
retaining too much so they don't exhale
20:41
too much compared to how much they took
20:43
in so it will measure that and what it's
20:45
measuring the two things mainly is it's
20:49
measuring the the fvc which is the
20:52
forced vital capacity and if they get a
20:55
low reading on this this represents
20:57
restrictive breathing and this is the
20:59
largest amount of air exhaled after
21:02
breathing in deeply in one second
21:05
another thing it looks at is it measures
21:08
the force expert ory
21:10
volume which is how much air a person
21:13
can exhale within one second and a low
21:17
reading will end
21:19
okay how severe the disease process
21:21
actually is so that is about COPD part
21:25
one now be sure to check out part two
21:27
and don't forget to take the in CLECs
21:28
review quiz that goes along with this
21:31
lecture and thank you so much for
21:32
watching and please consider subscribing
21:33
to this YouTube channel
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