This content provides a comprehensive overview of the acute management of asthma exacerbations, focusing on immediate treatment strategies to open airways, improve oxygenation and ventilation, and prevent further complications.
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Hey, this is Dr. Busty and we are in our
pulmonology section where we're going to
be doing a brief overview of the uh
management of acute asthma exacerbation.
I think it's important to recognize that
within this particular topic that if you
um haven't done so, it's probably worth
stopping and listening to some of the
background information or uh drug class
reviews for the different drugs or
agents because I'm not going to spend
time specifically going over the pharmarmacology
pharmarmacology
um and some of the main side effects and
those kind of things that we would
normally discuss in a drug class review.
So, those are made available. we do
provide those lecture topics and so I
just encourage you to know that
information as we move forward because
this is going to assume that you already
know some of that information and so
when somebody comes in with an acute
asthma exacerbation
um obviously they're short of breath
they're having difficulty with
oxygenation but even also some degree of
um ventilation oxygenation is getting
oxygen obviously from the air into our
blood and so it has to pass through all
the airways including the bronchules
into the alvoli so that it can exchange
and go and diffuse into the blood as
that's passing by. At the same time, the
blood is carrying endroducts of
metabolism, particularly CO2 that then
moves into the alvi and needs to be
exhaled out. That is ventilation. And so
when you start to have obstruction such
as an asthma exacerbation that can
happen, they develop these mucous plugs
um in pretty severe uh asthma attacks
that that then that plugged up area of
the airway cannot then not only get
oxygen but it also can't extract or
exhale off the CO2 and as a result of
that the patients can start to develop
um h become hypercapnic or hypercarbic
and these patients then go into
respiratory acid
as a result of it. And so our goal is to
open up those airways um to maximize
oxygenation and ventilation. And the
main stay of treatment in the acute,
right? Because there's not many drugs
that we have available that will manage
these patients acutely. But these are
the short acting broncoilators that are
listed here on this page. So we have
albuterol and epotroprium broomemide,
also known as atravent. Uh the obviously
the long acting agents aren't going to
help us. And in fact, if a patient is on
a long acting bronco dial beta aagonist,
uh, then that's actually a bad thing in
this situation. Uh, if patients are if
they haven't been on or they're already
on inhaled steroids, that's not going to
help us. You can give somebody
highdosese oral or IV steroids and we'll
talk about that here in a minute, but to
be honest with you, it's really not
going to help you in an acute setting
because those things are a delayed
onset. Um, so we have to think about how
we're going to open up those airways.
Then the first line therapy is
traditionally a combination of both
albuterol and uh epotropium or atrovent
both in pediatrics as well as adults.
Now the way you administer the
medication um is influenced by your
perception of the um literature uh and
your knowledge of the literature as well
as your own experience. Um if you look
up here you'll see that MDIs are
included in in this. So even a mendi
with a spacer four to eight puffs every
20 minutes for the next 4 hours or you
can use nebulizer solution and you see
that you give 2 to 5 milligs uh every 20
minutes for three doses. So we call that
stacking of the nebs and then you can
kind of start to taper out to every uh 1
to four hours as needed. But if you
can't get somebody to space beyond 4
hours then they usually need to be
admitted. Another option is just do it
via continuous uh usually sometimes
we'll use a positive pressure
ventilation system to uh deliver that or
you can just do it by a face mask
through nebulization. But the point here
is that MDIs or me doinators with a
spacer or nebulizer are pretty much
equally efficacious if you do them and
you implement them correctly. Um, and
the relevance of this is is that
patients outside of the hospital or
clinic environment can't carry and
generally don't carry a nebulizer
machine with them. So they need to know
how to use an MDI especially when they
get themselves in a difficult scenario.
Uh so the it is important to recognize
that the literature does support that if
you do it and you help the patient
through that process correctly.
Now when you consider eproprium comes
also an MDI as well as a neb and there
is duo nebs or comvent formulations
where they're formulated together. Now
when you look at these uh they're not
the same from the standpoint of their
pharmaccoinetic and dynamic profile. The
one problem with epotroprium compared to
albuterol is the epiropri has a delayed
onset maybe even up to 15 to 20 minutes
after administration but has a benefit
compared to albuterol in that epotropium
has a longer duration of action and so
that becomes somewhat relevant and we
think about it in this context here of
the pharmacocinetics. If you look at the
drug levels which then would exert some
pharmacologic effect over time here you
see that the albuterol which is the
darker uh you know line here starts
earlier usually within 5 to 15 minutes
uh but has a shorter duration of time
that it's that it's useful uh whereas
epotroprium as I said takes about 30 m
20 to 30 minutes or 15 to 20 minutes
before it actually starts to kick in uh
but lasts longer and so the duration is
longer. And so you create this overlap
uh where there's not only dual uh bronco
dilation happening but then there's a
continued bronco dilation effect
especially if somebody only got one dose
or the combo. And so the idea behind
this is that we stretch out the
broncodilatory activity from two
different mechanisms. Obviously beta
receptors and specifically the beta 2
receptors are being stimulated by the
alberol that increases cyclic AMP levels
that drives down cytoolic calcium causes
relaxation of the smooth muscle.
Epotropri is a muscerinic antagonist or
an anticolinergic um inhale uh
broncoilator and increases cyclic GMP
also driving cytolic calcium
concentrations down relaxing those
smooth muscle to broncoilate these
patients. Now steroids um are certainly
implemented but we we may give them
right when the patient comes in along
with these treatments. So treatments are
being stacked on top of each other,
right? You're doing multiple things at
the same time. But the reason that we
give them early is because there is a
delayed onset and we need to kick in the
drug as quickly as possible. Now the
problem within asthma is that there's
two phases of inflammatory response.
There's the acute uh sort of acute phase
reactions where there's the immune
system is initially spilling out all
these chemicals and mediators and then
there's the late phase which is where
there's this recruitment and the
migration of the white blood cells that
sets up the chronicity of a disease and
our goal in starting these is to try to
get a hold of that early phase and
prevent that late phase inflammatory
response from happening. So there is a
delay um but it's if by a few hours at
minimum. Okay. Now the way we administer
it is also very relevant and shows up on
Bor. There's really no difference in the
bioavailability whether you give it IV
or PO. Now here's the caveat. The caveat
is assuming that the patient isn't
nauseous and unfortunately steroids when
given by mouth especially on an empty
stomach can be irritating to the stomach
and cause nausea and vomiting. That's
not going to be helpful in a patient
who's in acute asthma exacerbation. The
other thing that's important to
recognize is that in a stressful
response, sometimes there's a
redistribution of the blood flow away
from the GI tract to more important
organ systems that are dealing with the
acute situation. And so therefore, the
the re the rate of absorption and the
overall amount that gets absorbed over a
period of a time may be affected by that
scenario. So most people in acute
situations, especially if you have
access to an IV or if you want to give
it IM cuz we do have IM steroids, then
that would be the way that some people
would do it basically to minimize
causing nausea, vomiting and or to not
worry about decreased potential GI
profusion in the context of a severe
asthma exacerbation. And one of the
other problems with aluterol is that
when you keep giving it, especially in
stack doses, that can make you also
vomit. And so we need to keep that in
mind and we don't want to cause another
problem because that certainly would
increase their risk for
aspiration. So if they're having
hypercarbia, right, retaining CO2 and
they're becoming hypercapnic or carbic,
then these patients are going to start
having an altered mental status. They
basically start getting very tired and
sleepy and they don't want to cooperate
and their mental status starts to
change. Well, you're not going to be
shoving oral medications down those
patients mouths because they're going to
be at risk for uh uh uh aspiration for
obvious reasons. Now, so predinazone or
predniscolone. Predinazone is the prod
drug prediniscolone. You can use either
one or methyl prediniscolone. If you're
going to use it IV, it needs to be the
suenate formulation. Whereas the methyl
prediniscolone acetate as a suspension,
it must be administered by IM injection.
Uh so you give it and you give it every
six hours um is typically how it's done.
Uh for pediatric p patients
prediniscolone again which is the active
form of predinazone 2 milligs per kilo
by mouth and we don't really need it for
that many days. Okay we're not looking
at chronic long-term use. Now, as I
mentioned at the beginning of this
lecture, especially in acute
exacerbation, we're trying to do
everything that we can to bronco dilate
these patients, prevent them from
obstructing and have it having mucus
plugging because then you can't
oxygenate or you can't ventilate. And
so, we really try to approach especially
in the more severe asthma attacks a
multiffactorial broncoilator properties.
So, this is where magnesium sulfate
infusions can be very helpful. Um again
if you think about knowing that smooth
muscle or any muscle has to have calcium
in the cytool for actinomyosin to
interact. If we can do anything to
reduce the amount of available mag uh
calcium present for actinomyosin to work
on then we're going to cause more
relaxation and more dilation. And so
when you think about that in the context
of magnesium calcium is a dvalent cation
but so is magnesium. And so what ends up
happening is they are magnesium competes
with calcium and functions kind of like
a calcium antagonist and as a result of
that magnesium can't be used by actin
andosin and so you get further
relaxation especially if patients are
not responding to initial um
broncoilatory pro uh uh medications. So
we usually give two this is adult dose
two to three grams IV over more rapid
infusion of 20 minutes. Um but you can
give it as fast as one gram per minute
um while the nebulizer treatments are
also going. So you have the ability to
do it. The point being is you want to
get them in because you don't really
don't want to intubate an asthmatic
because having them on a ventilator
causes a lot of problems in their
medical condition and it gets very
difficult to wean them off. Now what
about the use of recemic epinephrine via
uh nebulization? This drug was
historically used in the post-operative
setting to try to reduce oral like edema
uh from the endotrachial tube. Um and by
reducing the edema you could facilitate
sort of better air exchange and their
rapidity of re of recovery from the
post-operative from the operation so
that you can get them out. Well, so some
patients if they're having lurenio edema
or epiglatus that's edemmitus from the
endotracchial intubation or you have
swelling in that area recemic
epinephrine has been maybe potentially
helpful in reducing the amount of edema
and swelling in that area to maximize
movement. Why would it do that in any of
the tissue? Well, think about it.
Epinephrine works as a beta 1, beta 2,
and an alpha agonist. It stimulates all
of those receptors. And when you
stimulate the alpha receptor in
particular in this
scenario, you get vasoc constriction of
the blood vessels in that tissue. And as
a result, if you do have swelling and
you had edema and spasm and that because
of that adematus tissue, maybe that
epinephrine may constrict those vessels
and reduce the swelling. On top of that,
epinephrine stimulates the beta 2
receptors as well. And so but you know
that might add on some additional help.
So you get both broncoilatory effects as
well as the alpha 1 constricting
properties of the blood vessels in the
hopes that you reduce the swelling um
and edema around that area. Now you can
also administer it subcutaneously just
like you would for anaphylactic shock uh
for which is a type one hypersensitivity
reaction where we use the one to 1000 um
and you can administer it e or subq.
Now, if you're doing it IV, that
concentration is different, right? Uh if
you're doing it by nebulization, you you
pretty much put in.5 mls and you dilute
it up to 3 cm uh 3 mls of saline and you
administer over 15 minutes and you
repeat as needed. But that's when we
start to pull out that and this is
usually after people have already tried
epatropri and albuterol. They've already
been given magnesium. Okay, they're
still doing this. We don't want to
debate. We're trying everything we can.
And that's where maybe we start to
consider uh recemic epi knowing that
you're also going to get the beta 1
stimulation which is going to increase
your pulse which is also not sometimes
good. What about antibiotics? Should we
routinely start to use them? And the
answer is generally no unless you have
evidence for obvious infection or
pneumonia of some sort bacterial
infection in particular. And so usually
these patients are going to have a
fever. uh the white blood cell elevation
may be uh unreliable simply due to the
stress response of an asthma
exacerbation and depending on when you
draw the CBC in relationship of giving
the uh steroids. Steroids are known to
elevate the white blood cells. So you
kind of have to think about some of the
other things that would drive you to
want to use them but it should not be in
every single asthma exacerbation. But it
has some evidence in showing
improvements in symptoms and FEV1 which
is that forced expiratory volume in the
first second of exhalation and then it
may have some anti-inflammatory
properties. People tend to say that
about a zithroycin. The point being is
that you know if you reduce infection
you're going to reduce inflammation.
That's true for anything right? All
right. What about ventilation? So
remember I was telling you there's
oxygenation getting that oxygen down
into the alvoli so that you can exchange
and cause uh oxygenation to the blood.
Then there's the ventilation phase where
we try to exhale and get rid of
CO2. Um we tend to use or try to use
non-invasive ventilation. What I mean by
non-invasive is we're not going to do
RSI rapid sequence intubation where we
put an endotrachial tube down and
basically put them on a mechanical
ventilator. So our goal is to try to
avoid that with all cost. And so the
positive pressure ventilation or
non-invasive ventilation like BiPAP or
CPAP can be very helpful at maintaining
opening of those airways that are
spasming and trying to keep those alvei
open so that we maximize that gas
exchange. If we're going to have to
intubate the patient and undergo
invasive ventilation, then we need to
use the largest endotracchial tube
possible for that patient's age and
size. For an adult, if you can get an
eight or an 8.5 tube in, that's ideal
because again, trying to wean somebody
off of a ventilator and you're having to
breathe through a straw essentially. Uh
that's very that's very difficult. So
the bigger the straw, the easier it is
to breathe on that tube. So that's true
for any page of the patient. You always
want to try to use the largest
endotrachial tube that you can without
compromising the tissue or uh causing
trauma in the airway when you're placing
it in. We want to keep the peak plateau
pressures, that's the amount of pressure
that we're pushing in to be less than
30. And the reason for that is that we
don't want to put so much pressure in
the system to push those airways open
because then you can induce barrerow
trauma uh and that can lead to long-term
complications, remodeling of the airways
and also then start to even cause
inflammation itself. Helios is another
option that is sometimes used. There's
really no supporting evidence that it
should be used in all patients. Uh
however there are some again that just
are not responding where you again you
kind of think about it in the back of
your mind you pull it out. It is a
mixture of helium and oxygen and these
are the percents that you see here. Um
it works to replace basically the
nitrogen present in the air uh since
it's lighter in weight. So things move
around based on the density and that
makes it easier the theoretically easier
to breathe with less resistance to the
airways because remember we're trying to
maximize movement of air in and out and
so these are some of the things that are
sometimes utilized in there. Now again
through those ventilators and through
the non even the non-invasive we can
administer uh short acting uh bronco
dilators as part of this treatment. So,
you know, when we start somebody with an
acute exacerbation, we also need to be
thinking about what do we need to do to
transition them to the chronic phase
where we prevent that late phase
inflammatory response, but also try to
prevent the next asthma
exacerbation. And that's where looking
at um the adding on drugs and starting
them early in their process gets the
ball rolling. Not that they will stop
the acute exacerbation, but this
step-wise approach that's supported by
the GINA guidelines is really getting
patients geared now from an acute to
transitioning them to a chronic
maintenance phase. And you need to be
thinking about that early on. What drug
therapy do they need to be on? What were
they not on earlier that brought them
potentially in that caused that
exacerbation? So that that you can try
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