Hang tight while we fetch the video data and transcripts. This only takes a moment.
Connecting to YouTube player…
Fetching transcript data…
We’ll display the transcript, summary, and all view options as soon as everything loads.
Next steps
Loading transcript tools…
Session 2 - Live Rapid Review for BPS Exams | High-Yield Med Reviews | YouTubeToText
YouTube Transcript: Session 2 - Live Rapid Review for BPS Exams
Skip watching entire videos - get the full transcript, search for keywords, and copy with one click.
Share:
Video Transcript
Video Summary
Summary
Core Theme
This content is a rapid-fire review session covering high-yield immunology and cardiology concepts, along with pharmacogenetics, designed to prepare participants for board exams. The session emphasizes core principles, practical applications, and common clinical scenarios encountered in these medical fields.
Mind Map
Click to expand
Click to explore the full interactive mind map • Zoom, pan, and navigate
Well, welcome everybody. It's Dr. Busty
and Dr. Cookio. We are excited about
this uh session where we're going to be
covering and again rapid review format
the fire hydrant that is open and flowing.
flowing.
If you remember in the first session we
there was a lot of content probably a
little too much but that's all right. uh
we got through it and you guys uh were
good troopers and it's to your b
benefit. So uh but to this session is
going to be specifically about
immunology and thankfully from a high
yield core concept perspective there's
not many uh topics that are probably
going to hit on this uh for boards
pharmaccogenetics and we'll hit the high
points of those key um phcogenetic uh
variants that you need to know for drug
therapy. So it's again a short one and
then we're going to jump right into cardiology.
cardiology.
Cardiology just like other topics like
infectious disease and stuff are is a
fairly large topic but what we've tried
to do is put together again the top tier
high yield core concepts and make sure
we hit those uh key points. So we'll
follow a very similar uh format for the
most part and ensure that we have enough
time for questions and answers um at the
end. So, if you can try to hold off on
your questions towards the end, that
would be great. Um, the other if you do
encounter something or we something's
going wrong, you're not seeing
something, you know, certainly raise
your hand or make a send us a note or
chat uh and we'll be kind of monitoring
that. Dr. Kio and I uh will be doing
that together. For those of you that may
be attending for the first time, our
format here again is rapid fire. It's
not meant to be primary teaching. We're
hitting the core concepts. I will kind
of guide us to the initial disease
state. Then Dr. Kio will you know try to
put in a extra comment or two uh that
relates to certain ones that are more
applicable uh to board exams and but
keep in mind we're not going to talk
about minutia that's clinically relevant
but is never going to make it to a board
exam and that is content that's largely
of debate. It's going to be recognition
of a pattern of information that you see
um that leads to a most likely the right
choice of of a treatment or monitoring
parameter or management consideration.
So, having said that, we're going to go
ahead and and get started and and we're
going to start off with the most
difficult complicated
imunologic disorder on the planet that
makes everybody just nervous and shake
in their seat. And it's called allergic rhinitis.
rhinitis.
I mean, thank God, you know, this is a I
was kind of joking obviously, but you
know, allergic rhinitis does go through.
We got to keep learning fun, right guys? >> Absolutely.
>> Absolutely.
>> Um, but allergies are relevant because I
think we all at some level probably
suffer from some of them, some worse
than others. I know that I I encountered
that on occasion.
But we encounter an acute allergens and
then we sort of the body goes through
these various phases and what we really
want to prevent in in acute exposures is
the emergence into a long phase reactant
where there's this chronic symptoms and
that's where people feel tired and
fatigued and they have all these other
symptoms itchy you know uh their their
eyes itch their nose runs uh they may
scratch their skin in different places
those are the things that drive us
crazy. Um in the acute you know you see
sort of the vasogenic changes where
there's some edema runny nose congestion
uh so you know you get the rhinora and
then again the itching and sneezing
longterm it starts to wear it wear you
out and chronic chronic sort of symptoms
now what we're talking about is non type
one hypersensitivity reaction so this is
not an immediate hyper reaction uh that
you would see for anaphilaxis
um and so but we want to target even the
response to those early phases. So even
if it's not anaphylactic, we still want
to get that. So you know there's two
treatments, you know, antihistamines
which are only going to really work on
receptors that haven't been stimulated
by the histamine yet. Okay? So that's
why it's more preventative. It does help
in the acute, but it's really preventing
the further extre uh propagation. But
then uh intraasal steroids are really
the drug of choice uh in allergic
rhinitis. Nobody likes to squirt it up
their nose. It has it leaves a terrible
taste. Um it can lead to irritation,
nasal septal issues if you spray it
wrong. But by the evidence, it's the
stuff that actually works. Uh but who
want who wants to do that when you can
take a pill? Anything else?
>> I don't I I would Yeah, I mean with the
intraasal steroids, it it's such a
convenient over-the-counter therapy. I
mean I directly benefit from them myself
with allergic cryitis season but again
in my former training uh in Pra one this
actually came up this also related to
COPD maybe some asthma too related to
specifically HIV patients on proteiase
inhibitors there's a specific intraasal
steroid and also inhaled steroid
fluticazone that has uh therapeutic
interactions with protease inhibitors so
if I mean this is like a classic BECPS
or BPS exam question. If you had an
obvious patient with HIV on a protease
inhibitor and identifying the drug
interaction, but it's an inhaled
fluticazone. I mean, that would be a
slam dunk question in my mind because
it's a clinically significant
interaction truly um but some somewhazone
would not have that interaction. So,
it's a interesting therapeutic
interchange you can jump into.
>> I love it. All right. Now let's move on
to the acute sort of life-threatening
potentially situation that we do get
most concerned about and there are a
number of different instigators to
angiodma. So this is you know uh your
lips so the upper lower lip the tongue
and it can obviously affect the airway
which is why we get nervous and we
consider it a medical emergency in the
acute phase. But there's there's the um
uh hereditary form of angioadeema and
then there's sort of the ras mediated
which is really the kind of brada uh
ultimately being produced and then
there's idiopathic which um can result
from histaminic and other non-histaminic
pathways and so you get this painful
swelling uh that can be very concerning.
It certainly creates anxiety in the
patient and starts to look like
anaphilaxis. I mean it really does
outside of the um you know rash that
they form and the uh GI effects that
they uh usually don't see as much as
compared to aniflaxis but you know any
edema anywhere in the oral fairings can
extend down into the GI tract and cause
some nausea but what our biggest concern
is the airway. So, you know, there's
diff oops, sorry about that. There's
different treatments uh that you need to
recognize uh in the acute phase. A lot
of people want to throw all the an uh
anaphylactic treatments, the steroids,
the any benadryil and H2 receptor
antagonist, and quite honestly, those
really don't do that much um uh to
support uh the treatment of this. So
you've got uh calocrine and inhibitors
and you've got the bradaine two uh
antagonist like catabans is probably the
one for ACE inhibitor induced um
basically trying to block that bradakin
mediated vaso uh edema. So I don't know
if anything else you want to add there
Craig before we move on. Yeah, I mean,
yeah, these these cases are pretty
evident, but and again, clinical
context, those are uh hard to get
medications that can be highly
expensive, but I mean, it's a that or
intubation in these patients likely.
>> Yeah, if there's any compromise to the
airway and you feel like the airway is
going off, you have to intubate the
patient before it's too late.
>> Uh, all right. Psoriasis obviously a
more higher level alert you know
autoimmune kind of problem where we have
you know overly activated Tlymphosytes
and this causes a keratinic reaction
basically the keratinocytes are
replicating and they're overly
metabolically active which causes this
plaque formation on the skin. So you see
these plaques formation on the forearms
the shins the uh navis and the scalp and
it can be very irritating. Um there is a
a risk a sort of a scale that you can
use to help sort of quantify that. But
the common treatments that you would see
like if this is a first time diagnosis,
you don't always want to go straight to
the you know biologic agents. Those are
typically reserved for patients who are
more resistant. So um topical just
moisturizers, emollients can actually be
very effective if they're used
correctly. um topical corticosteroids
um you know depending on the surface
area that you're trying to uh to reach.
Um so those are probably the two most
common that you're going to see. Once
once patients um you know sort of fail
those initial topical treatments then
you're moving on to some of the
biologics or adding them on to as
adjuncts depending on how severe um they
tend to be. Uh anything else there
Craig? Yeah, that's a good summary of
that. All right. So, rheumatoid another
autoimmune disorder. But in this case uh
the now the cells and the we form
antibodies uh against uh portions of the
uh synovial membranes and so this causes
an attack of that and that affects the
synovial space and causes um
inflammation, irritation, fusions to the
joints and that results in uh basically
arthritis that's uh in in multiple
places and it's usually symmetrical and
that's important. It's not usually
isolated monoarthritic.
Uh it is symmetrical polyarthritic. Uh
they wake up in the morning very stiff.
Um and it sometimes takes them 30
minutes to an hour to get going. Uh
there are extra articular involvements
in some patients and those are what we
would see like with rheumatoid uh
nodules that can sometimes form. But
they need four of the following criteria
for at least six weeks. Um and again
morning stiffness lasting for at least
an hour. Swelling of three or more
joints again that's the polyarthritis.
Uh they have symmetrical involvement.
Rheumatoid nodules positive rheumatoid
factor is a prognostic indicator for the
severity. Uh but it's not always
positive in patients. So you can't rely
on that as a like rule out exam or test.
Um and then radiographic imaging like
X-rays can help you to see the arthritic
reactions and the swelling around the
joint space. um you're not doing it to
look to see if they actually have like a
fracture or dislocation. So early um and
probably a little bit more aggressive
treatment within that first three months
of the diagnosis considering
anti-inflammatory agents, analesics and
then demar therapy is very helpful at
preventing basically the structural
damages that cause patients to go into
contraurs have owner deviations um and
these types of things. So, you're
looking at higher dose prescription, you
know, appropriate anti-inflammatory
doses of NSAIDs, um, which then put the
patient at risk for gastritis and
potential kidney issues depending on if
they're bleeding risks and other drugs
thrown on board. That can be a problem.
Um, you know, you've got steroids that
can work because, as we know, the
problem with demar is that there's a
delayed onset. It doesn't, you know,
just happen like that. It may take
several weeks for those drugs to kick
in. So in the interim, the patient is in
pain, the patient has inflammation and
arthritis, and you want to do something
to treat that until these drugs start to
kick in. And then if you can wean those
down a little bit, that can be helpful.
Um, and so that's where we start
thinking of strategies of converting
people from NSAIDs to COX 2 inhibitors,
you know, uh, if you have more more COX
2 selective agents like, you know,
Moxyam, Dicloanac,
uh, you have your Celre still on the
market that you can and then use. And
then the next agent that is typically
added on as an adjunct is methtoresate.
And in that case you have to rule out
all the contrations. Are they pregnant?
Right? Or if female childbearing age
that becomes an issue. Uh their liver
function test in particular their renal
function um starts to play into that.
And so uh because the toxicity even
though we're dosing it very differently
than chemotherapy uh it still is
important. And so dosing of methtoresate
when you need to add it on is once a
week and it's a very low dose somewhere
between five and 10 milligrams a week
and you can give it through any route.
Once you go past that then you're
starting to get into the biologics which
many of them are the TNF alpha
antagonist. Uh Dr. Koko anything?
>> Yeah there I mean I think you did a good
description kind of escalating the
therapy uh to the demars and the
biologic demar. So uh but again the
highdosese NSAID is a typical therapy.
It's not your typical NSAID dosing for
muscular pain that we would normally
take. It's it's much higher. So, dosing
considerations with that would be relevant.
relevant.
>> Yep. Absolutely. All right. Good deal.
All right. So, lupus
uh so basically another kind of
autoimmune mediated you know we have B
cell T- cell activation uh where these
um you basically have these antibodies
that kind of can bind
antifphospholipids. It triggers
different cytoine release. it certainly
activates compliment and then you get
this cascade which actually can put the
patient also at risk for clots. Um so
it's a kind of a syndrome which is when
you look at some of the clinical
presentation um you have mucosal
involvement you have joints involvement
you can have vascular involvement um and
it's not um easy to make this diagnosis
um it is actually very difficult to do
so we do have lab tests which you know ANA
ANA
uh uh test uh that's anti-uclear
antibbody test and anti- double strand
DNA antibodies anti-smith antibodies and
anti phosphoippids are things that are
commonly assessed in those patients. But
I'll just say again, just like with
rheumatoid and rheumatoid factor, it's
not always 100%
positive and sometimes you see
variation. And so you have to combine
the clinical with the iminologic
criteria to kind of guide you uh to the
diagnosis. And so that's where we have
this um sort of you know you you take a
certain number
um of agents or in the criteria in those
two groups and you um consider them kind
of similar to things like uh um Duke's
criteria and stuff like that where
there's major and minor criteria. You
you have to consider multiple. I don't
think I don't think the board exam would
make you memorize that. They'd rather
probably give you those work up and that
there's concern for the diagnosis. That
would not be your focus. Um and so given
the more involvement of both B cell T-
cell activation you're going to go to a
little bit uh you know riskier agents
you know like anti metabolites dear
therapies corticosteroids
uh certainly uh through exacerbations
you can get cycloposomide rettoximab are
fairly common in the more resistant or
acute um um cases. The big thing that
you want to watch out for is lupus
nefritis in these patients outside of
clotting. Um so if they develop
antifphosolipid antibodies they can
stroke have DBTs pees you know just like
anybody else. Um and so this requires
anti-coagulation therapy which is not
technically listed here but if they do
have antiphospholipid antibodies they
are problematic u in that anything else there
there
>> uh just a quick drug induced cause of it
that might be relevant to acute care
folks is a procanomide.
>> There you go. Even though
>> Yeah. Yeah.
>> Yeah. The oral is oral is still gone.
Not we don't have that in the United
States. Like we don't use it chronically anymore.
anymore.
>> I haven't seen that. Yeah.
>> Most of it's um intravenous or parental
use for acute cardiac dysriythmias but
uh yes it's a classic sort of link to
it. All right. So acute on chronic graph
versus host disease. These are patients
that basically have a transplant of
imunologically competent cells into an imunompromised
imunompromised
host. So right we you know imunino we
suppress the patient's immune system as
they receive a transplant so that they
don't reject it but the cells that are
coming in could obviously go against the
host. Um and so you know there's
different phases they go through as they
enter into the length of the graft. Um
and so just keep in mind there's three
of those phases uh there. And so the
acute induction um is a little bit more
aggressive so that we prevent that
initial shock of the exposure and then
there's the post-transplant where
patients are on traditional agents uh
many times in combination with each
other depending on the type of organ
that is being transplanted. Um and you
have corticosteroids, calcinurine
inhibitors, calcinurine inhibitors being
your cycllosporin, your tacro and your
uh mecholymus. And then you have your
mTor inhibitors like erolymus and
cerolymus uh that are also many times um
used and so uh big issues with them
toxicity side effects kidneys insulin
resistant blood pressure issues anything
else Craig
>> no I mean just a highly complex issue
but yeah the drug therapy is pretty
intense uh for these patients but it's a
huge risk benefit scenario because the
grapher's host disease could be certainly
certainly
>> devastating catastrophic Yeah,
>> especially after all the effort.
>> Um, but just make sure you know the
monitoring parameters, side effects. I
don't think they're going to ask you
like drug levels necessarily because it
varies the time on the organ. All right,
so that was immunology. So now we're
going to kind of jump into
pharmaccogenetics and genomics. And so
just as a quick overview, uh, you know,
obviously the human genome project has
been done for quite a while. And part of
that project of mapping out each of the
chromosomes and the DNA is that it
creates an address or a map of the of
each chromosome and you break it down
into its nucleotides. And what we found
is essentially we all pretty much are
the same except we vary by uh snips or
single nucleotide polymorphism. So each
one of these letters if you remember
back from the old biology days not to
cause PTSD in anybody um but those are
individual nucleotides. You have
guanine, adinine, thymine, cytosine. You
know, remember the, you know, talking
back and forth, GC, AT, and then you
have every three you have a codon. So,
when you think about what happens when
DNA unravels, we uh read it and we
capture a copy uh through an RNA strand.
So that messenger RNA then goes out into
the cytoplasm and it goes to the
messenger RNA I'm sorry to the um
cytoplasmic reticulum and where there
are different ribosomes present um and
they read them and so just like if you
were to cook a cake or you know bake a
cake or you know make something you're
going to read a recipe. So you're
reading the instructions and every three
nucleotides represents a codon sequence
and that codon sequence that you can see
here as it moves represents what amino
acid would be placed in that portion or
that position of the chain. So if you
change one of these letters single
nucleotide polymorphism you then change
the codon when you change the codon you
then chair for change which amino acid
gets placed at that position. and you're
like, "God Lee, this is so small. Who
cares?" Uh, the reality is each one of
these um uh amino acids carry different
charges and dipole moments and all these
things that cause, remember, as we form
uh a protein, it goes through its
primary structure, which is basically
what number four is, the string, and
then it starts to fold and shape and
create a three-dimensional structure,
and you go to secondary and tertiary and
even quartinary effects, which create
pockets and binding pockets. And if you
just change any bend, you could change
the position of that pocket just enough
that affects the binding affinity or
even the activity uh of this uh protein.
So for example, if there's a truncation
uh or stop codeodon, uh you might not
make the full cake, right? You've only
made the batter. I mean, batter's pretty
good, you know? I mean, I could probably
stop right there and just eat the
batter, right? But I mean, when you put
the you know, cook it and you put the
icing on it, it's even better, isn't it?
Uh, in most cases, and all of y'all want
some cake.
But when we get these snips is what we
call them, they uh obviously are wild.
They're they're variations from the wild
type. Wild type being the general
population, the normal common uh
genotype that you see. But when you have
a variation, it's usually represented
with an italics and then this sort of um
asterisk with a uh number behind it. And
really what that is is just kind of
really alerting you. This isn't
intuitive like oh that means that at you
know at position 636 there's a guanine
converted to an edine and that changed.
You know you can't discern that. You
have to kind of memorize the genetic
polymorphism. But what it does is it
links to an address. So, think about the
internet and your computer. We all each
computer right now, all of you on have
an IP address somewhere in the worldwide
web. And it's no different than your
home address or a business's address.
It's a location. And if you, you know,
get that number wrong and you put it in
your GPS, you show up at the wrong spot.
And that's kind of what's going on here.
So, this trying to, they're trying to
codify for you what it means. So at
position n 636 of the nucleotide list
there's a guanine switch from an adinine
and that changes the amino acid that was
normally tryptophan at position 220 212
to a a termination sequence. So this
truncates this particular
uh protein and it renders it essentially
inactive. So it doesn't work. So if you
got a drug that gets metabolized by 2C19
and you have asterric 3, well nothing's
going to get metabolized through that
pathway. So what are the most common um
sort of linked patterns of association
that you would be asked that are not
only in the guidelines, so they're well
established, but they're also
recommended on product package insert
recommendations or FDA approved
recommendations. Um and the first one is
a NNRTI
known as Abakavir.
This is your HIV anti-retroviral drug
therapy for uh HIV infection. And when
patients have HLA, which is more of the
immunologic genetic variation, uh 5701.
Okay. And you just got to memorize these
if this is new to you. For those of you
that have been around this a little bit
longer, this probably no big deal. But
for those of you, this is new. You need
to memorize it. You just got to memorize
it. Go into the exam, write it down on
your cheat sheet, and regurgitate it.
Uh, but this results in what's called a
hyper uh a back of your hypersensitivity
reaction, which is really a
constellation of symptoms. Um, and just
like a most hypersensit hyper
sensitivity reaction, have pulmonary
manifestations and develop fevers, um,
skin rashes and these types of things.
Um, Dr. Cookio, I mean, please chime in
if there's anything else you want to add
on any of these here. Um, alo puridol,
uh, this is one of your xanthine oxidase
inhibitors for the treatment of gout.
Uh, HLA 5801. So, you can see where it
gets a little confusing, like if you're
on a board exam, you don't want to get
these numbers flipped in your head. Oh,
which one is it? 57 or 58 because both
are going to be listed. You know that,
right? Um, so, so you just, that's what
I'm saying. Memorize it, regurgitate it.
And these are more problematic in
patients with CKD and of Asian various
Asian descents or ethnicities. Um, and
I've seen this actually happen. This is
this is almost like a TEN looking syndrome.
syndrome.
>> Uh, basically uh TEN being toxic
epidermal necrolysis or basically a bad SJS,
SJS, >> right?
>> right?
>> So remember SJS is less body surface
area. TENS is a more significant body
surface area. It's really just the
amount of they're both the same problem.
Carbomasopene or tegrl HLA B1502
again SJS TN and the Han Chinese in
particular uh clitigril
2C19 uh you know asterisk 3 here or star
three reduce platelet inhibition because
remember clitigil is a prod drug it
requires two levels of functional
activation before it works. So if you
want antiplatlet properties or effects,
this is one of those situations where it
has to get metabolized.
Um and so is the same thing with
prazigril. Um the only one that doesn't
have that issue is ticloral out of the
uh glyoprotein two. Uh wait a minute, no
no yeah no p2 y12 receptor attack. >> Right.
>> Right.
Keep it all straight in your heads.
Right. This rapid fire gets a little
tongue tied. I run a tan. This is one of
your chemotherapy anti-neoplastic drugs.
I ran to the can, right? Diarrhea,
severe, but that's the dose limiting
toxicity in chemotherapy. When you've
already proven the patient doesn't have
this genetic polymorphism. If they have
a phase 2 metabolic pathway polymorphism
like UGT 1A1 star 28, these patients
basically can't metabolize the drug and
it shunts it basically down its anti
anti- uh uh or
uh uh imunosuppressant effects and it
basically suppresses the bone marrow and
cause severe neutropenia. They actually
have a um um point of care test that you
could theoretically do in clinical
practice. And then lastly, our favorite
and and most common drug that we just
love and we wish would stay on the
market forever is warfern poison. Um
that is uh where we have two genetic
polymorphisms. one to vcore which is
your vitamin K epoxy reductase inhibi
inhibition and then there are the enzyme
that basically uh gets it reactivated um
and then your metabolism pathway
remember a warin is a recemic mixture
you got an r isomer and an s isomer the
s isomer predominantly is metabolized
via 2c9 so if you do something to affect
it you impact the efficacy and
anti-coagulation of of potency of bas
basically of the uh warfin. So if
there's actually more polymorphisms that
make it work too well, so it chews it up
basically, rapidly metabolizes it and
doesn't work. So they need higher doses
and then if it doesn't work as well,
then they're obviously at higher risk uh
for uh bleeding. Anything else to add
here? Yeah, I mean I would just echo a
lot of what you were saying that uh I
mean even for the case of a backir I
mean a with with some of these
polymorphisms they require pre-esting
before we can actually start drug
therapy so a backer would be in that uh
in that realm whereas other drugs like
like you were mentioning with warin or
even clipidil we don't necessarily
empirically test for these atoms so on a
test question you might see an adverse
event and have to equate it back to
warfin but again with a back of your you
would have to have the test before you
actually start drug therapy. So just a
consideration and applying that both
clinically and also on the test.
>> Agreed. That's very that's an excellent
point um to add as to how to how to
interact with the question what they may
be asking you to do because you're right
not a lot of these are tested in
clinical practice. Um I just want to say
there there is one of you on here Amanda
is a huge fan of Warren. So shout out
Amanda. Go girl.
I'm with you. Rat poison all the way.
I'm just kidding.
>> I like reversing it.
>> I like reversing it. There you go.
That's the fun part. Okay. So So we are
doing good. So like I've committed to
you, we're we're hanging out. I just
want to pause here since we are on time
and we're now heading into the
cardiology which is a a larger uh
section. So we have more slides to go
through. Um, I want to just make sure
does anybody else have any questions
because this is a good time if you want
to ask a question about immunologic
disorders or pharmaccogenetics or genomics.
Okay, looks like maybe we
we have one
uh someone else just agreeing that they
love Warframe. Uh, will board exams be
given um brand or generic names? And the
answer is generic. Yep.
>> Very rarely will you ever see on any
board and that's true for even the board
exams. I mean I took you know in nursing
and medicine and it was always always
that. Now you know obviously pharmacy is
more prone to needing to know both but
and I don't think it hurts you
clinically to know that but u okay so so
someone's asking here Miranda asked do
we need to know the star three or is
just the 2C19 polymorphism enough? The
2C19 polymorphism is enough. The UGT181
star 28 is enough. The HLA5701,
that's all you need to know. You don't
need to know anything beyond that like
what's the address, what amino acid,
>> true replaced. They're not nobody unless
you're a pharmaccogenetics expert uh is
going to know those things. That is
clinically also irrelevant.
>> Uh what sometimes is relevant is to know
that some of those have more than one
genetic polymorphism and 2C19 is one of
those. 2C9 is another one. 2D6 has
multiple genetic polymorphisms. And what
I mean by that is um the um uh some some
are more uh you're a fast metabizer and
some you're a slow metabolizer. So it
just varies. Um so there's a again Craig
jump in anytime here. I don't
>> All right. So there was a question about
yes is Moxyam also a COX 2 selective and
Jennifer the answer to that question is
yes um so when you look at um there it's
not listed as a COX 2 inhibitor but it
is more COX 2 selective and what does
that mean? COX 2 selectivity has to do
with the COX 2 to COX one ratio. So when
you look at and it will depend on what
paper you read but the overwhelming
amount of evidence would suggest there's
a pattern even though there's variation
there's a pattern that moxyam
uh dicloanac
um tend to be slightly more in the cox 2
inhibition still has cox one and you
know if you think about aspirin it's
basically cox one especially platelet
cox one getting platelet don't express
COX 2. Um, so when you look at them,
you're looking at that the what's the
ratio? And so if you can't get access to celoxib,
celoxib,
uh, the next best agent is Moxyam or
Mobic. Okay. Uh, Craig, anything to add
on that? I don't know.
>> No, no, I think that was a good summary.
>> All right. Uh, Amanda asked, "Is
hydraazine still on the SA SLE list?"
And that is an excellent question,
Amanda. Thank you for asking it uh
because the answer is yes. Uh where it's
becomes relevant is in high doses uh
chronically uh but yes that's uh
possible uh one on there um you know you
know uh procanomide which we would still
use in patients with like uh aphib with
RVR or in patients which we'll talk
about here in a minute and WPW in particular.
particular.
>> Yeah. Um all right so could you please
get go into the pharmaccogenomics of
warfin okay so there are two
uh enzymes that are impacted as it
relates to warerin there's vcore okay
which is the the enzyme vitamin K
epoxide reductase so if you think about
it it's basically reducing vitamin K
back so that it can be used in the
process of glucar
um adding a um a
caroxile group to the structure that
basically facilitates the functional
activation of the clotting factor. So
remember when you make clotting factors
in the liver they're not active they
have to get activated functionally
activated and that's what vcore is
doing. So there are there are genetic
polymorphisms to vcore. So it impacts
that. Okay. And that's what that's what
warfrint is inhibiting vcore that is the mechanism.
mechanism.
The S isomer is more potent at doing
that. Okay. That means you don't have to
the amount is that's needed to inhibit
is not very much compared to R isomer.
Now when the you have the S and the R
isomer, they are metabolized through two
different pathways. S isomer is
predominantly through 2C9. the R isomer
is through 3A4.
So that's where the variations that we
see in rat poison use um is due to the
fact that patients have genetic
polymorphisms at multiple isoenzymes 2C9
3A4 vcore and it's very difficult to
predict unless you have that information
ahead of time and there are institutions
that do that there are advanced
practices that actually genotype
patients and know that and there are
calculators that you can plug in the
genotype of the patient and spit out a
starting dose but at the end of the day
you just have to adjust test it. >> Mhm.
>> Mhm.
>> Um All right. Could you repeat the risk
of lupus complications, clots and um so
it's multic.
So it affects joints, the vascule,
uh uh muc various mucous membranes and
things like that. And so they have a lot
of skin manifestations, vascular
manifestations. They can have arthritic
reactions. They can also because of the
vascular effects can also affect their
kidneys. um and the vascular flow
through that. So that's what lupus nefritis
nefritis
ultimately ends up being. Um and so the
clotting really comes up from anytime
you inflame or irritate the
endovvascular lining, you increase or
precipitate platelets being activated
and the clots coagulation cascade
kicking on. when uh you have
antifphospholipid membrane or
antifphospholipid antibodies which is a
component of lupus uh that can form u or
antifphospholipid syndrome which I think
comes up actually in the next section um
then these patients need to be on anti-coagulants
anti-coagulants
uh all right so let's see is asking uh
how should we differentiate between RA
and OA in treatment modalities excellent
question. So is there a blood test for
OA like there is RA? And the answer is
no. So RA is primarily a clinical diagnosis.
diagnosis.
So that's why you have to look at those
four criteria being present for at least
six weeks for RA. And if you have
rheumatoid factor positive lab test,
it's helpful, but it's not an absolute
like you can't just rule it in and rule
it out purely based on that. So it's a
clinical combined with a laboratory
diagnosis. OA the RH factor should be
negative and typically it's not the
same. You have no extra articular
involvement. So not um these rheumatoid
nodules don't show up and things like
that. Uh an OA tends to be weightbearing
joints, the knee, the hip, uh shoulder,
cervical spine, those kind of things.
does tend to be the ones that are from
use overuse whereas rheumatoid is a
autoimmune mediated problem. I hope that
was helpful. Uh what about acetilators?
Are we talking about acetilators for Jennifer?
Jennifer?
Oh, fast and slow acetilators. Okay, so
that would be in the context of inh
inh
uh in particular. Um so people that are
at risk for uh neuropathy associated
with uh INH and if I'm not mistaken it's
the fastelators. I don't know Craig
maybe you might can't remember.
>> I don't remember exactly related to that.
that.
>> I think it's where you ex you're doing
it too much and it can pass through into
the brain. Um
or maybe it's the slope. I I have to
double check. Maybe we have to look at
it during the break.
>> I'll have to look that up.
>> Um sorry about that. But that's a great
question uh Jennifer uh as it relates to
acetilation would be predominantly inh
or isized and the risk of neuropathy.
Uh the difference between uh SJS and TN
um is it Premlana I think is okay. I
hope I just said your name right. Uh we
don't give I'm not saying your last name
so no one knows who you are but but um
differences between uh Stephen Johnson's
and TEN. All right. All right. So these
patients develop rash throughout their
body. But remember both SJS and TN will
have mucosal involvement. So the
conjunctiv of the eyes inside the nasal
naries your mouth you can oral fingial
involvement. Um for women the vagina uh
for men the ure urethral opening and
also urethral opening for uh women. So
you have to kind of look in those
places. Um so that's where the rash is.
The difference between SJS and um um
um >> TN
>> TN
um is um is body surface area. How much
of the body surface area? So TEN is
typically over 30%. That's what most
people would say.
>> Yeah, that's what I say.
>> Yeah. SJS is there's a little fuzzy gray
zone between I think like 10 and 20 or
I'm sorry 20 and 30 that like is this abyss.
abyss.
>> Yeah. Uh but anything less than uh or 30
is typically more SJS mediated and
Amanda the rockar helped us out and
double checked.
>> Thank you Amanda our colleague
in the background. Uh she checked and
it's slow acetilators. Uh and that would
make sense I guess now that I think
about it. I I had a little TIA. Um and
um but yeah, so you're not metabolizing
it. So it obviously penetrates the
central nervous system a little bit more
readily. But you know who who on earth
do you know is a slow acetilator. So
until we get you know pharmaccogenetic
testing that allows us to basically do a
genotype analysis on patients
um you know where we do a profile just
like a CBC or chemistry at the beginning
of a workup you know we're we're left
out here. So I that probably is the
future. you'll probably order a CBC,
Chem 7, you know, get a year analysis
and get a genotype because it will be
that easy uh in the future and
cost-effective to consider and then
it'll spit out these are the drugs just
like a culture and sensitivity. These
are the drugs to give, these are the
drugs not to give.
>> That'd be nice.
>> I mean, really, I mean, it's true, right?
right? >> Absolutely.
>> Absolutely.
>> All right, guys. Those were rockstar questions.
questions.
>> Yeah, absolutely.
>> I I think you guys are just awesome.
>> So, thanks for participating. Um I
promise to give you a um moment to
stretch and do DVT prophylaxis and make
sure and ensure that none of you develop
decubitous ulcers. Um so we will do that
here in just a few more minutes. All
right. So let's move into some
cardiology. All right.
Uh hopefully some of y'all smiled at
that little joke.
All right. Breda cardia slow
pulse, right? Yeah. I mean, basically
there's something affecting the heart
rate and it's, you know, most commonly
by definition a diagnosis where the
pulse is less than 60. Okay. But why is
it drug induced? That's easy, right? So
look for drugs that are nodal blocking
agents. Okay. Um do you have something
that has impaired the SA or AV node i.e.
you get an insult like basically heart
attack you know you can have a clot of
of you know one of the coronary vessels
that supplies the nodes basically do
that so you then you start seeing
depending which node is affected
especially like the AV node that's where
you start to see uh first and second and
third degree heart block uh depending on
the degree or involvement and what then
it does to obviously uh the correlation
to Pwaves in relation to QRS's U and so
you know you know first degree is you
know you sort of just have this
prolonging of the PR interval second
degree you have different two different
types and it's not necessary for your
boards and then third is sort of this
wandering pacemaker it's just they're
not talking to each other anymore um so
some people can be asymptomatic or just
not feel like great to actually having
syncopy all right uh because they get so
brada cardartic that if especially when
they change positions they get
orthostatic and then uh they get they
don't have enough blood flow or
compensatory mechanisms to raise the the
the pulse to generate increased cardiac
output to peruse their brain and so they
get lightheaded, dizzy with changes in
position um in particular. So you want
to try to identify the reversible causes
and like in my world of practice in
emergency medicine if someone comes in
with acute unspecified brada cardia I
have to be strongly concerned that's not
an MI uh because you know that because
that if I sit there and waste time uh
now the cells are dying right so that's
you have to be really careful in
considering what that is and if they
become symptomatic where they're not
perusing their brain then you've got to
increase that pulse
So the quickest, fastest way to do that
is to throw pads on them and start
transcutaneously pacing them. Now that
isn't comfortable or fun having just you
know thing, you know, I mean shocking
you. So you've got to provide the
patient with analesia. If you have
access to an IV and you don't have the
pads available quickly, then you know
atropene epinephrine are your go-to
agents and you should you know try to do
that especially if the brada cardia is
also associated with hypotension uh
epinephrine can be uh beneficial. Craig, anything?
anything?
>> Yeah. Uh I mean that's a great analysis.
I mean one thing with atropene again we
want to make sure that we're
definitely I mean it's quite considering
like you think it's not relevant but
being in that clinical environment
myself seeing that in reality it is it
is pretty uh hard to perceive but I mean
even sedating these patients uh while
keeping them conscious is something you
can try but you're still limited because
they're probably bradic cardartic
probably not
>> blood pressure yeah they're probably
hypotensive so it's a complicating
factor you can at least try to give them
certain opioids that aren't going to
affect the vascule like uh fentanyl if
you can. Um but it's a really
complicated issue with atropene too. I
know we don't always focus on dosing for
board certification exams like this
scenario. In this scenario, I think you
would uh for the purpose of whether the
patient has a pulse or not. So if they
have a pulse, the dose is lower for
atropene being 0.5 milligrams. So it's
something you would at least
hypothetically consider um >> absolutely
>> absolutely
>> to at least be relevant in that in that
context. And then you could do IV pushes
of epinephrine or an infusion which is
probably more relevant for these patients
patients
>> at least.
>> And the other thing to consider here is
the brada carar is not from tox right.
Absolutely. If you got, you know,
calcium channel blocker like a non-digit
periodine calcium channel blocker
overdose, you know, dioxin overdose or
beta block overdose, then you need to be
actually thinking of the antidotes, but
they're going to give you on the boards
some indication or concern that there
may have been a bottle of drugs. You
know, there's they're going to lean
towards the tox scenario, but you got to
keep in the back of your mind,
especially when patients aren't
responding appropriately. Um uh so Betsy
did chime in and tell us that she's
going to need paste during the exam.
I just had to share that in the context
of our brain cardia. And then Dena says,
"Yeah, we could also use dopamine, you
know, from the 1830s." And you know
what? Actually, that's it's a it if you
if you don't have access to certain
medications, and this is where you need
to know alternatives,
>> and dopamine um actually could be an
agent that you would consider using. So
that's not actually 1830s. It may not be
the first easy go-to and it's certainly
not the cor most correct answer uh on
the test but definitely something to uh
>> to you know consider. So thanks for
actually adding that pulseless
electrical activity. This is PA arrest.
So this is basically cardiac arrest
>> pulseless. You don't have a pulse that
you can palpate. You probably don't have
enough blood pressure and perusion that
goes to the noggin. So you are unresponsive.
unresponsive.
Right? And so remember when you're in
cardiac arrest where ACLS is being
implemented, if you look up on the
monitor or on the you know the the
defibrillator and your p you're watching
the rhythm and you see during the pulse
checks that there's clearly an organized
rhythm but you can't feel a pulse or
palpate a pulse in the central areas
then that patient is not perusing their
brain which is why they're unresponsive.
U and that's basically it. Now I'll put
you down a pathway which is different
than pulseless VTAC and VIB and that's
key because that's where your
anti-ythmics are going to work. That's
where your defibrillator works not in
PA. Okay. So cardiac arrest unresponsive
no spontaneous uh respirations in most
cases and these patients end up needing
you know ventilation support whether
it's intubation or bagging or uh and
then they need chest compressions uh
with good CPR. That's why you see here
listed ACLS protocol, chest
compressions, uh intubation, or
ventilation, whether it's a um sort of a
a king airway or something where they
just, you know, throw something in
temporarily um or you're doing BVMs um
whatever. It doesn't matter. Good chest
compressions is the only thing probably
out of everything in here that's going
to matter. Now with PA you need to think
and also consider underlying reasons why
are they in PA and that's where the five
H's and the five T's that we always talk
about sort of become um the things you
go through and I actually in the code
will say okay team
>> what are the five H's and the five Ts
and are we missing something here what
have we not given or considered in this
situation especially when the patient
isn't clearly responding and I don't
have a history. All right, those five
H's are hypoalmia. So give them fluid,
maybe they can't fill a pulse because they're
they're
>> volume depleted, hypoxia, so that's
where the airway comes in, especially in kids.
kids.
>> Um they're in acidotic state, they have
a hypo or hyperclemic state, hypo or
hypothothermic state. Um and then
hypoglycemia and then the T's are
tensionthorax or uh cardiac tampenod
where the the swelling is and the fluid
in the around the membrane of the heart
is just basically compressing on the
mioardium and it's not able to squeeze
massive PE. Okay. And this is the one
that I've seen enough to where you
actually need to be thinking tpa
>> in these patients. So if you got any
indication of a recent surgery,
hypercoagul disorder, if you can glean
any information that suggests that and
this patient is otherwise normal or
healthy, you're right or you know
functional at least, you don't want to
just quit the code. You really want to
consider TPA. Will it save them?
I've only seen it get rosque in my
personal experience once or twice. Um,
but most of the time when it's not
worked, it's because the the time that I
got to them or they arrived was so long
that even the PE the PE was too
devastating that u we couldn't recover.
>> I already agree. Yeah.
>> Um, but yeah, so when you see here you
got epinephrine, you got atropene and
the dosing of atropene being different
um we what what Dr. Kokio was talking
about uh lidocaine, amiotarone only if
you start to flip into more so if you
because people will go in and out. >> Yeah.
>> Yeah.
>> Uh VTAC VIB. So remember really kind of
think of those more of the because VTAC
VIB is really truly probably more of a
vascular problem, you know, heart
disease problem. Um this can be from a
whole lot of things that aren't
necessarily vascular disease. Anything
else? Uh Dr. Koko here?
>> Yeah, I would just echo in on that. uh
PE uh I've seen a lot myself clinically
where it's uh you know young person with
other eyes unknown medical history but
you know as the pharmacist and the team
just being able to recall certain drug
therapies that you know patients might
be on if you recognize any anti-diabetic
agents maybe make sure they get a finger
stick so we can check glucose you know
certain interventions for uh potassium
uh you know it's just a component of
that we can contribute when we're you
know participating in a code it's
certainly valuable but uh yeah I've
experienced Same thing with the the pees
and arrest.
>> So basically, so there was a question
about patients having just baseline
brada cardia. Sure. I mean we're talking
about symptomatic brada cardia guys
symptomatic. If you're not symptomatic
then leave it alone.
>> Don't do anything. Now you may still
explore it. I've seen patients with
first and second degree heart block
>> that are mildly asymptomatic and you
don't do anything to those patients. You
just get them to cardiology
>> and to explore a reason why. Um but
we're talking about more symptomatic um
someone again you asked this question I
think last time about by carb and
hypocalemia and I I think we addressed
that uh it's not a common um
a common thing that that I'm aware of
except that when you you cause somebody
to go alkalotic
theoretically you're going to uh drive
potassium inside the cells and so If you
check a serum potassium level,
theoretically that's one of the
treatments of hyperc >> calalemia,
>> calalemia,
>> but I I I would not hyperfocus on that.
I think you've asked that twice. I I
would totally dismiss that from a board
exam perspective, >> right?
>> right?
>> Pulseless VTAC VIB. Again, you don't
have a pulse and you're unresponsive.
So, the same problems. They need chest
compressions um and they need uh CP uh
chest compressions with some sort of
airway support. Um and then there's um
uh patients you basically initiate ACLS.
Now this is where amiotto and lidocaine
kind of the anti-ythmics sort of pop up
and it's really after you've gone
through two full rounds of CPR before
you're really kind of thinking in that
direction. But man, if you have the
treatment choice and it is
defibrillation, not cardio version guys, defibrillation,
defibrillation,
>> right? Mhm.
>> electrical defibrillation. They probably
will put on their cardio version to see
if you know the difference. Cardio
version is in patients with sustained VTAC.
VTAC. >> Mhm.
>> Mhm.
>> So that you time the generation of the
of the electrical surge basically at the
right time in the cardc so you don't
flip them into uh ventricular dysriythmia.
dysriythmia. >> Right?
>> Right?
>> Whereas defibrillation it just slams it
right then and you have a fibrillating
ventricle. You're trying to reset the
pacemakers essentially. Totally two
different things. So, make sure you
don't screw that up. Okay. >> Absolutely.
>> Absolutely.
>> Uh I don't have anything else to add
here except that you don't see atropene
here and you uh and I would just suggest
that too much epinephrine. My personal
clinical I shouldn't even go on. This is
a board exam review. It's epinephrine test.
test.
>> Clinically clinically epinephrine's not
helping them. Okay, move on. Great. Uh,
anything else?
>> I mean, again, I could go on a long
tangent, but uh, I think for purpose of
the board exam, I think this is spot on.
>> Yeah. All right. Yeah. I'm sorry, guys.
We have to stay focused on the board
exam. We don't want to get into the fact
that you should also consider Esmal
drips. Oh,
>> that's what I was talking about. That's
what I was going to talk about.
>> I can't believe it.
>> Ignore that. Do not give Esmal on the
board exam
>> or dual field relation.
It's fine.
>> Okay. All right, guys. Sorry, we
couldn't resist.
>> We're a little little bit of adrenaline
junkies here, I guess. So,
>> all right. Sustained VTAC. So, what does
that mean? Well, you have consecutive
ventricular beats essentially or PVCs
that are in a run. So, I mean, you see
the VTAC
on the screen and you're like, uh uh, is
the patient awake? If the patient's
talking to you and they have BTAC on the
monitor, make sure there's not some
attending physician taking the uh
electrode and going like this and
looking around trying to get, you know,
the the novice
clinician to to go into a seizure. I'm
just kidding. I've actually done that.
Play jokes, but
you can create VTC by doing that. Don't
do that. um nurses will run in the room,
slap you in the face and all the
>> All right. Anyway, so rule out the
physician number two, but uh if they're
talking to you and they're awake, then
that means they're profusing their
brain. Even if they have a pathologic
cardiac dysriythmia on the monitor, you
don't treat monitors. You treat the
patient with a disease and you consider
the monitor.
So, so the reason I say that is your
approach is very different. Right now,
if these patients obviously with a
sustained VTAC, you're not getting good
profusion to the brain. You can
obviously increase the oxygen demand on
the heart that certainly puts the
patient at increased risk of myioardial
eskeemia. So, that can then induce
another problem and then they can flip
into pulseless VTAC or VIB. So, you
don't want them to go that direction.
So, I'm not saying, you know, sit down
and have a glass of wine with them. At
the same time, you, you know, be okay
and just get things rolling to try to
slow it down and or convert them
pharmacologically if you can. If they
are starting to have symptoms, i.e.
chest pain, i.e. starting to like
they're talking to you, but they're not
their blood pressure is dropping and
they're hypotensive. Their systolic in
the 80s and but they're still there. You
got a pulse. You're not in cardiac
arrest yet. You synchronize cardiovert
that patient. Screw amiiotarone.
Period. Right? If you have the ability
to get the amiotone, you're going to
tell the nurse, "Go get the amiotarone.
Just get the bag ready. Get the drip
going. Go pharmacy. Whatever you need to
do, get it in here. But put the pads on
the patient and get them ready for a
cardio version. And I'm sorry, you just
got to do it." >> Yep.
>> Yep.
>> And it's going to hurt and they aren't
going to like you. Uh, if it's a good
old boy redneck,
they might come jumping off that bed
after you afterwards. Seen that happen
once before.
I do. If it's a big old boy with big old
muscles, I always go, "Sir, I hate to
tell you this, but this is going to
hurt, but it's for I'm gonna save your life."
life." >> Yeah.
>> Yeah. >> Sorry.
>> I told you.
>> It's true. It's true.
>> I mean, you just have to do it. And if
you sit there and you jack around with
it too long, patients either gonna die,
flip, or you know, they're gonna start
getting anxious. Just do it.
>> All right. And then they'll they will
feel better and you can calm them down
quickly after that. All right.
>> All right. Sorry. SVT
supra ventricular. So above the ventricle
ventricle
is some originating tacocardia but it's
stimulating the ventricles because
you're seeing a pulse that is can many
times be up into the almost 200s. >> Mhm.
>> Mhm.
>> Okay. So basically um
um
there's uh two paths of electrical
circuits that exist essentially and
they're not responding appropriately.
Right? So normally like your AV node
would theoretically regulate those.
Okay. Um and so it's not working for
some reason or it's too overstimulating
the the ventricles. So SVT uh when they
come in many times they are awake but
again they're still in the same dilemma.
If they start having chest pain running
beats of a 180 to 200 220 beats per
minute you can't sustain that for a long term.
term.
Um, so these patients start getting some
chest discomfort. They can start having
lightheadedness. Uh, they can start
having dysmia because they're not able
to get good forward flow. They can go
into heart failure if it's left
untreated for too long. Now, most
patients, especially if they have the
diagnosis, they know it and they know
what to do.
>> Um, so you get an AKG, you put them on a
monitor and you see that just narrow
complex just
not not the tech, okay? not a wide QRS
complex, but you have a narrow QRS
complex and it's just usually about 180
to 200 beats per minute. So, the
quickest, easiest thing to do is if
they're hemodynamically stable, i.e.
blood pressures, systolics and adults
are still over 90, they're not having
active chest pain and they're not
becoming lethargic, then you do the
valva maneuvers on them. Okay? I'm
talking significant vala maneuver. Not like
like
like no like
>> you're gonna go all out baby here. You
mean I and I get yelling at the coach and
and
>> I give them a syringe. I take the
plunger off and I said or I pull the
plunger back it out. I said I want you
to blow that plunger and hit it all the
way to that wall over there. Go. And I
mean I'm yelling at them
>> and they just turn bright red in the
face because I want them to not have to
get adenosine. >> Yeah.
>> Yeah.
>> But if that doesn't work and they're
still stable. Okay, hemodymodynamically
stable. Then we go to the denosine
route. If they become unstable for any
reason, it's again cardio version, not defibrillation.
defibrillation. Cardio version.
Cardio version. >> Very important. I could see that being
>> Very important. I could see that being potentially asked of you.
potentially asked of you. >> If you give a denosine, you need to
>> If you give a denosine, you need to recognize that the halfife of the drug
recognize that the halfife of the drug is literally like 10 seconds. So, if you
is literally like 10 seconds. So, if you administer it because you got some
administer it because you got some rockstar nurse who knows how to feed a
rockstar nurse who knows how to feed a catheter through the finger vein, okay,
catheter through the finger vein, okay, that's probably not going to make it in
that's probably not going to make it in 10 seconds all the way into the heart,
10 seconds all the way into the heart, right? So, you want the most proximal
right? So, you want the most proximal portion and you want it in a big IV with
portion and you want it in a big IV with a stopcock and a and a and a push 20
a stopcock and a and a and a push 20 cc's of normal saline at minimum.
cc's of normal saline at minimum. And you want to raise that arm up. You
And you want to raise that arm up. You slam it in six milligrams. You follow
slam it in six milligrams. You follow with 20 cc's while they're on the
with 20 cc's while they're on the monitor. They will usually become very
monitor. They will usually become very brada cardartic. Sometimes have a
brada cardartic. Sometimes have a cardiac pause and then that will usually
cardiac pause and then that will usually bring them out. Thank god that the
bring them out. Thank god that the halflife is only 10 seconds because that
halflife is only 10 seconds because that cardiac pause could remain permanent,
cardiac pause could remain permanent, right? So we don't want a drug sticking
right? So we don't want a drug sticking around for a long time. If that doesn't
around for a long time. If that doesn't work, you can attempt a 12 milligram
work, you can attempt a 12 milligram because essentially what you're
because essentially what you're concerned about is it's metabolizing.
concerned about is it's metabolizing. I have never needed to use 12. You do it
I have never needed to use 12. You do it right. Craig, anything else here?
right. Craig, anything else here? >> Uh yeah, I mean I I've seen a lot myself
>> Uh yeah, I mean I I've seen a lot myself the val maneuver. I would agree. I I've
the val maneuver. I would agree. I I've never seen it work when we just did the
never seen it work when we just did the simple gentle uh maneuvers, but the more
simple gentle uh maneuvers, but the more I I don't even want to call them modern.
I I don't even want to call them modern. I think they're like original like those
I think they're like original like those maneuvers and then inverting the
maneuvers and then inverting the patient's legs and have them laying back
patient's legs and have them laying back down as soon as you get them to blow the
down as soon as you get them to blow the syringe. That seems to work. Uh in my
syringe. That seems to work. Uh in my experience, I've had a denazine drawn up
experience, I've had a denazine drawn up because I'd never seen it work and then
because I'd never seen it work and then it started working a few times in a row.
it started working a few times in a row. Uh but yeah, denazine like you're
Uh but yeah, denazine like you're mentioning, make sure I mean we try to
mentioning, make sure I mean we try to slam it in uh to get it to the heart so
slam it in uh to get it to the heart so it can work before it's eliminated.
it can work before it's eliminated. That's a key factor. Um, I mean the
That's a key factor. Um, I mean the doses that you see are the recommended
doses that you see are the recommended doses, but again clinically they can go
doses, but again clinically they can go both higher and lower depending on drug
both higher and lower depending on drug interactions, but I mean they're they're
interactions, but I mean they're they're those are somewhat
those are somewhat >> six milligrams is the first dose. That's
>> six milligrams is the first dose. That's what that's your board question
what that's your board question have on the monitor. You cannot give it
have on the monitor. You cannot give it in a clinic. You need to have cardiac
in a clinic. You need to have cardiac monitoring because the risk is cardiac
monitoring because the risk is cardiac arrest. That's why we do it emergency
arrest. That's why we do it emergency department settings if these things.
department settings if these things. Okay guys, we're going to take a at
Okay guys, we're going to take a at least a five minute
least a five minute uh break here. Why don't we stretch DVT
uh break here. Why don't we stretch DVT prophylaxis and um decubitous ulcer
prophylaxis and um decubitous ulcer prevention and we'll come back and we'll
prevention and we'll come back and we'll hit unstable anga.
hit unstable anga. So we're going to pause the screen here
So we're going to pause the screen here for a second and we'll be right back.
you back? >> Oh, yeah. I'm back.
>> Oh, yeah. I'm back. >> Cool.
Amanda said, "Take your Warframe." That's right. Except Warfin, you know,
That's right. Except Warfin, you know, takes a couple days to kick in, right?
takes a couple days to kick in, right? Stuff sucks,
Stuff sucks, >> right?
>> right? Amanda's my new friend.
Amanda's my new friend. That's good.
That's good. All right,
Amanda, where are you at? Like, where do you where do you practice
Like, where do you where do you practice or like what city?
or like what city? Oh, cool. My family's from there.
Stephen, my my my hospital's finally getting rid of deol after a thing.
getting rid of deol after a thing. Oh man, 89year-old OB. Oh my gosh,
Oh man, 89year-old OB. Oh my gosh, that's cool.
that's cool. I love PA.
I love PA. Okay, guys, we're going to get started
Okay, guys, we're going to get started back. Hopefully everybody's back and uh
back. Hopefully everybody's back and uh got blood flow going and you're you have
got blood flow going and you're you have a pulse and uh not in cardiac arrest if
a pulse and uh not in cardiac arrest if you need to give yourself chest
you need to give yourself chest compressions.
compressions. Just kidding. All right. Uh let's talk
Just kidding. All right. Uh let's talk about some unstable anga and STEMI. So
about some unstable anga and STEMI. So basically this is a vascular problem. Uh
basically this is a vascular problem. Uh usually from aththeroscotic plaque not
usually from aththeroscotic plaque not rocket science. Not trying to insult
rocket science. Not trying to insult anybody's intelligence here. Uh the
anybody's intelligence here. Uh the types of symptoms that people uh you
types of symptoms that people uh you know typically express are more adult
know typically express are more adult men just to be honest with you. The
men just to be honest with you. The classic you know chest pain, pressure,
classic you know chest pain, pressure, you know, lavine sign and you know
you know, lavine sign and you know radiation to my left shoulder and
radiation to my left shoulder and nausea. You know to be honest with you
nausea. You know to be honest with you women about onethird of women will
women about onethird of women will present in an atypical presentation. Oh
present in an atypical presentation. Oh I got indigestion belching. Uh you know
I got indigestion belching. Uh you know I just don't feel right. I mean, weird
I just don't feel right. I mean, weird stuff. So, you gotta people that in that
stuff. So, you gotta people that in that age group with risk factors got to keep
age group with risk factors got to keep in mind for board exams, they're going
in mind for board exams, they're going to be very classic presentation of the
to be very classic presentation of the leftsided subternal chest pain or
leftsided subternal chest pain or pressure. Uh, usually associated with
pressure. Uh, usually associated with some nausea, shortness of breath. It'll
some nausea, shortness of breath. It'll be pretty obvious. Now, in STEMI means
be pretty obvious. Now, in STEMI means that on an EKG, you don't see the ST
that on an EKG, you don't see the ST segment elevation. So, it doesn't meet
segment elevation. So, it doesn't meet the criteria of STEMI. Okay? But
the criteria of STEMI. Okay? But everything else matches up. If they
everything else matches up. If they present early on they may not have
present early on they may not have elevated troponins because it can take
elevated troponins because it can take up to six to 12 hour six to nine hours
up to six to 12 hour six to nine hours for a tropponin to become positive. It
for a tropponin to become positive. It has to do with the assay. Do you have a
has to do with the assay. Do you have a highly sensitive tropponent or not? So
highly sensitive tropponent or not? So there's a lot of things that go into
there's a lot of things that go into interpretation of the lab. But the point
interpretation of the lab. But the point of the matter is for ST segment or
of the matter is for ST segment or non-ST segment elevations you could have
non-ST segment elevations you could have inverted T- waves you could have ST
inverted T- waves you could have ST segment depressions.
segment depressions. Okay. And an unstable anga is different
Okay. And an unstable anga is different where you have chest pains and all the
where you have chest pains and all the symptoms
symptoms might have some EKG subtle changes but
might have some EKG subtle changes but they're not in a pattern but the
they're not in a pattern but the tropparonin is normal. There's no cell
tropparonin is normal. There's no cell death. So just because someone's
death. So just because someone's tropponin is negative doesn't mean that
tropponin is negative doesn't mean that they don't have an athoscorotic problem.
they don't have an athoscorotic problem. Okay that's really important. Um so what
Okay that's really important. Um so what do you do? Um, so aspirin obviously and
do you do? Um, so aspirin obviously and it's aspirin with really in the first 24
it's aspirin with really in the first 24 hours of the onset of symptoms. There's
hours of the onset of symptoms. There's really no value or benefit giving to
really no value or benefit giving to them right away when they first walk in
them right away when they first walk in the door. In the first 30 seconds do
the door. In the first 30 seconds do don't even talk to them. Just give them
don't even talk to them. Just give them the aspirin. That isn't going to change
the aspirin. That isn't going to change anything. The ISIS 2 study didn't show
anything. The ISIS 2 study didn't show that the time of administration in
that the time of administration in relation to the time of onset of
relation to the time of onset of symptoms change the outcome. As long as
symptoms change the outcome. As long as you gave it in the first 24 hours,
you gave it in the first 24 hours, um you reduce vascular related mortality
um you reduce vascular related mortality by 20 20 to 23% at 30 days. If you have
by 20 20 to 23% at 30 days. If you have an STEMI unstable anga, you really
an STEMI unstable anga, you really should probably be considering some
should probably be considering some anti-coagulation
anti-coagulation um in this situation. There's a lot of
um in this situation. There's a lot of debate about anti-coagulation and
debate about anti-coagulation and whether it has benefit or not. Um but
whether it has benefit or not. Um but the if you have basically certainly if
the if you have basically certainly if troponent is a posit they're having
troponent is a posit they're having positive symptoms you need to be going
positive symptoms you need to be going to that because they probably need to
to that because they probably need to have a cardiology consult probably need
have a cardiology consult probably need to go to kath lab. Uh oxygen is only to
to go to kath lab. Uh oxygen is only to be used if they're hypoxic.
be used if they're hypoxic. In fact oxygen administration during and
In fact oxygen administration during and stemi and stemi when you don't need it
stemi and stemi when you don't need it has been shown to worsen outcomes. Uh
has been shown to worsen outcomes. Uh nitroglycerin very rarely is beneficial.
nitroglycerin very rarely is beneficial. um it doesn't mean anything if you give
um it doesn't mean anything if you give it to them and their chest pain goes
it to them and their chest pain goes away diagnostically that means nothing
away diagnostically that means nothing you just their chest pain is gone um so
you just their chest pain is gone um so aspirin I'm sorry nitroglycerin use um
aspirin I'm sorry nitroglycerin use um has never been studied in acute coronary
has never been studied in acute coronary syndrome as we administer it sublingual
syndrome as we administer it sublingual five uh every five minutes times three
five uh every five minutes times three has never once been studied ever uh to
has never once been studied ever uh to my knowledge I've never found a
my knowledge I've never found a reference to support it it's
reference to support it it's extrapolated information. So, it's a
extrapolated information. So, it's a non-evidence-based treatment that really
non-evidence-based treatment that really doesn't have any validity. And if you
doesn't have any validity. And if you have a right-sided MI could actually
have a right-sided MI could actually worsen the patient's clinical condition
worsen the patient's clinical condition and deteriorate them. So, be very very
and deteriorate them. So, be very very careful if you're going to give
careful if you're going to give nitroglycerin that you've ruled out type
nitroglycerin that you've ruled out type five phosphorus inhibitor use. Uh
five phosphorus inhibitor use. Uh whether it's being used for pulmonary
whether it's being used for pulmonary hypotension or erectile dysfunction.
hypotension or erectile dysfunction. Craig,
Craig, >> yeah, I mean, I would echo that. Uh just
>> yeah, I mean, I would echo that. Uh just those small things. I mean even though
those small things. I mean even though nitroglycerin as you mentioned similar
nitroglycerin as you mentioned similar to aspirin as soon as chest pain hits
to aspirin as soon as chest pain hits the door they might get it.
the door they might get it. >> Yeah. Um the other thing is if someone's
>> Yeah. Um the other thing is if someone's got true salicellate or aspirin allergy
got true salicellate or aspirin allergy that you want to basically go to
that you want to basically go to clopidigil. Um so just another point
clopidigil. Um so just another point here. Uh so signs and symptoms. Jennifer
here. Uh so signs and symptoms. Jennifer is asking what are the signs and
is asking what are the signs and symptoms of a right-sided MI? So think
symptoms of a right-sided MI? So think about right-sided heart failure and
about right-sided heart failure and think about right-sided MI. There's very
think about right-sided MI. There's very similar pattern. Now on an EKG, there is
similar pattern. Now on an EKG, there is a particular distribution
a particular distribution uh that would help you see it. You're
uh that would help you see it. You're not going to be asked that on the board
not going to be asked that on the board exam. You it's totally irrelevant for
exam. You it's totally irrelevant for you. U they'll just say there's concerns
you. U they'll just say there's concerns for or they'll give you the diagnosis
for or they'll give you the diagnosis based on EKG findings or something like
based on EKG findings or something like that. You're not going to know or it may
that. You're not going to know or it may require Kath lab to know. Um however if
require Kath lab to know. Um however if you have the EKG pattern that is
you have the EKG pattern that is concerning then they're preload
concerning then they're preload dependent essentially. So anything that
dependent essentially. So anything that reduces preload or vasoddilates the ve
reduces preload or vasoddilates the ve veins uh is going to worsen their
veins uh is going to worsen their outcome. So they're preload dependent
outcome. So they're preload dependent and that's where nitroglycerin is
and that's where nitroglycerin is problematic in these patients.
problematic in these patients. >> In fact you might even give them a
>> In fact you might even give them a little bit of fluid if they're not you
little bit of fluid if they're not you know in fluid overfail. But what are the
know in fluid overfail. But what are the signs and symptoms? So think of it right
signs and symptoms? So think of it right side heart failure. You can see JVD
side heart failure. You can see JVD distension. you can start to see backup
distension. you can start to see backup in the periphery, but again, it's acute.
in the periphery, but again, it's acute. You're probably not going to see edema
You're probably not going to see edema and things like that because it's not
and things like that because it's not going to happen that fast,
going to happen that fast, >> especially if they're presenting with
>> especially if they're presenting with you in to you within a specific time
you in to you within a specific time frame. STEMI, on the other hand, is
frame. STEMI, on the other hand, is really more of a full vessel occlusion.
really more of a full vessel occlusion. Um, and these patients, like when you
Um, and these patients, like when you see a STEMI, you won't forget it. Um, I
see a STEMI, you won't forget it. Um, I mean, these patients look very sick.
mean, these patients look very sick. They look like something's wrong. They
They look like something's wrong. They look like they're going to die. They
look like they're going to die. They have that dusky appearance.
have that dusky appearance. >> It is not a good situation. I mean, I
>> It is not a good situation. I mean, I can walk in the room and go, "Uh oh,
can walk in the room and go, "Uh oh, this is not well. This is I mean, I
this is not well. This is I mean, I don't even need to ask a question like
don't even need to ask a question like that does not look right."
that does not look right." >> So, they're you very sweaty. Most of the
>> So, they're you very sweaty. Most of the time they're they can they will be
time they're they can they will be vomiting. Um because the anxiety gets
vomiting. Um because the anxiety gets them so worked up um and then their
them so worked up um and then their hypoprofusion starting to have
hypoprofusion starting to have hypopusion and they just get sick and
hypopusion and they just get sick and then they start vomiting which is
then they start vomiting which is actually stressing them more. Um so
actually stressing them more. Um so which then becomes a problem because how
which then becomes a problem because how are you going to give them aspirin? So
are you going to give them aspirin? So that's where you need to think of
that's where you need to think of different dosage formulations and give
different dosage formulations and give it rectily u because we don't have IV
it rectily u because we don't have IV aspirin in the United States. Outside
aspirin in the United States. Outside the United States they have IV aspirin
the United States they have IV aspirin but not here. Um you start thinking
but not here. Um you start thinking started anti-coagulation make sure you
started anti-coagulation make sure you can if you can try to get them clipil
can if you can try to get them clipil that's helpful. Uh depending on where
that's helpful. Uh depending on where you're at you're activating the kathlab
you're at you're activating the kathlab or we call it stemi activation. Um now
or we call it stemi activation. Um now the the considerations is timing right
the the considerations is timing right so if they're within 12 hours of the
so if they're within 12 hours of the onset of these symptoms then you can
onset of these symptoms then you can consider tpa in the pathway
consider tpa in the pathway assuming you've ruled out contrations
assuming you've ruled out contrations and you have no kath lab within the next
and you have no kath lab within the next you know you can't get them into the
you know you can't get them into the kath lab in the next with with
kath lab in the next with with angoplasty within the next 90 minutes if
angoplasty within the next 90 minutes if you can't do that then these patients
you can't do that then these patients need to you know you need to give them
need to you know you need to give them the litics and get them out of there
the litics and get them out of there >> so if you're in a if they give you a
>> so if you're in a if they give you a setting where you're in the rural
setting where you're in the rural community environment and you don't have
community environment and you don't have an active kath lab or the kath lab is
an active kath lab or the kath lab is closed, you have to think
closed, you have to think non-conventional.
non-conventional. Go back to the old days. Okay? And
Go back to the old days. Okay? And that's where tpa comes back up again.
that's where tpa comes back up again. >> Um and so you got to remember these
>> Um and so you got to remember these little indications like with PE, massive
little indications like with PE, massive PE, submassive pees, uh obviously es
PE, submassive pees, uh obviously es schemic strokes and then STEMI within 12
schemic strokes and then STEMI within 12 hours of onset of symptoms without
hours of onset of symptoms without contraations.
contraations. All right. Now in STEMI they obviously
All right. Now in STEMI they obviously have ST segment elevations and it's in
have ST segment elevations and it's in two contiguous leads which means there's
two contiguous leads which means there's it's in the same pattern of distribution
it's in the same pattern of distribution of the uh assessment of that pattern of
of the uh assessment of that pattern of blood flow into the heart of that
blood flow into the heart of that particular area like the anterior uh
particular area like the anterior uh ventricle posterior you know aspect or
ventricle posterior you know aspect or inferior locations based on the coronary
inferior locations based on the coronary distribution. Um so these patients
distribution. Um so these patients should get aspirin quickly. um whether
should get aspirin quickly. um whether you use a noxoparin or unfractionated
you use a noxoparin or unfractionated hepin is going to be influenced
hepin is going to be influenced uh the or by valin is influenced by the
uh the or by valin is influenced by the geographic practice patterns. Any one of
geographic practice patterns. Any one of those answer choices are legitimately
those answer choices are legitimately correct. If the board exam puts all
correct. If the board exam puts all three on there, that would be a a bad
three on there, that would be a a bad question because they're all legitimate
question because they're all legitimate and they're all endorsed by the
and they're all endorsed by the guidelines. Mhm.
guidelines. Mhm. >> Um, so you have to consider either and I
>> Um, so you have to consider either and I don't think they're going to give you
don't think they're going to give you doses personally,
doses personally, >> but this is the one situation if you use
>> but this is the one situation if you use Lovvenox that you can give a bolus dose
Lovvenox that you can give a bolus dose IV push. So it's initial 30 milligrams
IV push. So it's initial 30 milligrams IV push followed by subcutaneous
IV push followed by subcutaneous injection. That's the only kind of weird
injection. That's the only kind of weird situation in that.
situation in that. All right. What else Craig? Anything
All right. What else Craig? Anything else? You actually mentioned uh ABSAB
else? You actually mentioned uh ABSAB earlier instead of a vakavir. So abs is
earlier instead of a vakavir. So abs is one of the GP2B3A inhibitors. So a key
one of the GP2B3A inhibitors. So a key caveat with that is essentially patients
caveat with that is essentially patients can only get it once. So if they've ever
can only get it once. So if they've ever had a previous MI with a cath and got
had a previous MI with a cath and got absab, they'd have inifacttoid reaction
absab, they'd have inifacttoid reaction the second time they got it from
the second time they got it from antibodies that developed to it. Uh but
antibodies that developed to it. Uh but it's rarely ever used in cathods, but
it's rarely ever used in cathods, but you still it might be a relevant uh you
you still it might be a relevant uh you know patient history factor that you
know patient history factor that you might have to consider suggesting
might have to consider suggesting different cathode strategies. uh with
different cathode strategies. uh with the I'm glad you mentioned the anoxipar
the I'm glad you mentioned the anoxipar dosing because that is somewhat relevant
dosing because that is somewhat relevant to um that has come up. Um morphine is
to um that has come up. Um morphine is something that is interesting. I don't
something that is interesting. I don't know how much that'll come up on the
know how much that'll come up on the boards, but there's concerns that it
boards, but there's concerns that it actually increases mortality. Um,
actually increases mortality. Um, there's some varying theories behind it,
there's some varying theories behind it, either masking the pain, so the
either masking the pain, so the perception of the severity of the MI is
perception of the severity of the MI is declined, but also a potential drug
declined, but also a potential drug interaction with uh the cliprell or any
interaction with uh the cliprell or any of the other uh activators that it'll
of the other uh activators that it'll since it a 2D6 inhibitor might prevent
since it a 2D6 inhibitor might prevent some of the activation to its pro uh
some of the activation to its pro uh from its prod drug to its active drug.
from its prod drug to its active drug. So it's somewhat controversial to give
So it's somewhat controversial to give although I still see it clinically and
although I still see it clinically and it's uh
it's uh >> it's bad habits.
>> it's bad habits. >> Yeah, it's
>> Yeah, it's >> people don't know the evidence.
>> people don't know the evidence. >> Yeah, it's complic it's complicated.
>> Yeah, it's complic it's complicated. >> If you look at all subcohorts of
>> If you look at all subcohorts of analysis of and stemi patients that
analysis of and stemi patients that >> Yeah.
>> Yeah. >> they looked at this, they all have worse
>> they looked at this, they all have worse outcomes with morphine.
outcomes with morphine. >> All and there seems to be some effects
>> All and there seems to be some effects on the platelets that Dr. Kio was
on the platelets that Dr. Kio was talking about that seem to be playing
talking about that seem to be playing into that. Plus, it's the lack of
into that. Plus, it's the lack of perception because you've treated their
perception because you've treated their pain and somehow they're now better. So,
pain and somehow they're now better. So, I tend to avoid morphine. I don't like
I tend to avoid morphine. I don't like the Mona acronym for treating STEMI uh
the Mona acronym for treating STEMI uh and and STEMI patients. I don't believe
and and STEMI patients. I don't believe in that because oxygen shouldn't be used
in that because oxygen shouldn't be used in most patients
in most patients >> and nor should be not not always
>> and nor should be not not always nitroglycerin and not morphine. So,
nitroglycerin and not morphine. So, really it's aspirin
really it's aspirin >> pretty much pretty much. Okay.
>> pretty much pretty much. Okay. >> Pretty much. And then one last thing
>> Pretty much. And then one last thing with the with the thrombolytics. So
with the with the thrombolytics. So similar I think we talked about with PE
similar I think we talked about with PE um that the you start hepin if you start
um that the you start hepin if you start a hepin in a patient and they're a
a hepin in a patient and they're a thrombolytic candidate you essentially
thrombolytic candidate you essentially don't hold the hepin uh which completely
don't hold the hepin uh which completely contrasts what you are used to with a
contrasts what you are used to with a stroke patient where they don't even get
stroke patient where they don't even get DVT prophylaxis for 24 hours which is
DVT prophylaxis for 24 hours which is not something that was actually based on
not something that was actually based on the clinical evidence as something based
the clinical evidence as something based on practice since you look at the
on practice since you look at the nittens trial they actually got DVD
nittens trial they actually got DVD prophylaxis at day so in contrast again
prophylaxis at day so in contrast again just think about it if they got heperin
just think about it if they got heperin is not a contra indication uh to
is not a contra indication uh to thrombolix for a STEMI or a PE.
thrombolix for a STEMI or a PE. >> Very good. Excellent. All right. So,
>> Very good. Excellent. All right. So, there was a quick question while we're
there was a quick question while we're on these. Why does STEMI PCI have a time
on these. Why does STEMI PCI have a time limit but N semi doesn't? Well, part of
limit but N semi doesn't? Well, part of it's a pathology. If you have full full
it's a pathology. If you have full full vessel occlusion and you don't open that
vessel occlusion and you don't open that vessel up, that tissue is definitely
vessel up, that tissue is definitely going to die and probably going to flip
going to die and probably going to flip into pulses vacry bib. Um so they want
into pulses vacry bib. Um so they want to open that vessel up and preserve the
to open that vessel up and preserve the eskeemic penumbra essentially. Um and
eskeemic penumbra essentially. Um and that's where the evidence lies. Um so
that's where the evidence lies. Um so there was a question also about the
there was a question also about the anti-coagulation. Um they should not in
anti-coagulation. Um they should not in a STEMI a offer you uh which of the
a STEMI a offer you uh which of the following is should you start next and
following is should you start next and have lovox unfractionate hepin by val
have lovox unfractionate hepin by val ruden and I mean you you can't pick
ruden and I mean you you can't pick between those three. They're all three
between those three. They're all three unless it's all the above. I mean but
unless it's all the above. I mean but you wouldn't start all three at above
you wouldn't start all three at above but any of the above I mean would be
but any of the above I mean would be accurate, right? So that's not even an
accurate, right? So that's not even an option. Whoever wrote the question
option. Whoever wrote the question clearly doesn't understand anything if
clearly doesn't understand anything if it happens. Um and you should be
it happens. Um and you should be concerned that the exam is not valid. Um
concerned that the exam is not valid. Um so uh and there's no real generally
so uh and there's no real generally there's no dosing in most cases but the
there's no dosing in most cases but the administration or root or approach could
administration or root or approach could be uh testable uh Dena. So basically if
be uh testable uh Dena. So basically if if they put on there uh like lovox with
if they put on there uh like lovox with initial IV push dose that's very
initial IV push dose that's very appropriate. They may not give you the
appropriate. They may not give you the dose even though it's 30 milligrams.
dose even though it's 30 milligrams. It's pretty easy. It's only one
It's pretty easy. It's only one situation where you do it anyway. Um,
situation where you do it anyway. Um, but anyway, all right, moving on. Keep
but anyway, all right, moving on. Keep us moving so we don't get behind. Um,
us moving so we don't get behind. Um, because I'm answering probably a little
because I'm answering probably a little bit too many questions here, but I want
bit too many questions here, but I want to I know you guys are trying to learn
to I know you guys are trying to learn as we go. Uh, so cocaine induced MI. Um,
as we go. Uh, so cocaine induced MI. Um, so this is not an athoscotic problem and
so this is not an athoscotic problem and so don't treat it like an athoscotic
so don't treat it like an athoscotic problem. Okay. Uh, I'm not saying that
problem. Okay. Uh, I'm not saying that cocaine users don't have athoscerosis
cocaine users don't have athoscerosis and if they do then certainly consider
and if they do then certainly consider that. But most cases these are
that. But most cases these are vasospasms
vasospasms um typically um and so these vasos
um typically um and so these vasos spasms can cause typical chest pain they
spasms can cause typical chest pain they can have a heart attack elevated
can have a heart attack elevated troponins EKG changes just like
troponins EKG changes just like everybody else and so the drug of choice
everybody else and so the drug of choice is not like hurry up get the aspirin
is not like hurry up get the aspirin it's actually give them a benzoazipene
it's actually give them a benzoazipene Adavan um you know IV uh IV Adavan is
Adavan um you know IV uh IV Adavan is actually one of the recommended uh
actually one of the recommended uh treatments and it's something if they
treatments and it's something if they still don't get some resolution, then
still don't get some resolution, then you want to consider something that will
you want to consider something that will reduce some of the vasospasms.
reduce some of the vasospasms. Okay? And um so nitroglycerin can be
Okay? And um so nitroglycerin can be helpful in that situation. Um it's
helpful in that situation. Um it's pretty easy to use. Many times their
pretty easy to use. Many times their blood pressure is already elevated
blood pressure is already elevated anyway. This will help reduce the the
anyway. This will help reduce the the the blood pressure. It will also relax
the blood pressure. It will also relax the coronary spasms. Um and you know,
the coronary spasms. Um and you know, benzoazipines will bring it down. It's
benzoazipines will bring it down. It's not intuitive to think of
not intuitive to think of benzodazipines, but think about what's
benzodazipines, but think about what's happening with cocaine. It goes into
happening with cocaine. It goes into your brain and prevents the re-uptake of
your brain and prevents the re-uptake of norepinephrine and dopamine. So your
norepinephrine and dopamine. So your sympathetic outflow from your brain is
sympathetic outflow from your brain is high
high high. All right? And so on top of that,
high. All right? And so on top of that, if you can calm them down and and get
if you can calm them down and and get them to relax a little bit, you reduce
them to relax a little bit, you reduce also the sympathetic tone. Hopefully you
also the sympathetic tone. Hopefully you can relax these vessels and reduce the
can relax these vessels and reduce the spasm. Um, and obviously if they have
spasm. Um, and obviously if they have underlying disease, because I've seen
underlying disease, because I've seen older patients in their 40s and 50s,
older patients in their 40s and 50s, 60s, 70s use crack and cocaine. It's not
60s, 70s use crack and cocaine. It's not >> Yeah.
>> Yeah. >> Not just 20 year olds. Uh, I mean,
>> Not just 20 year olds. Uh, I mean, >> don't stereotype everybody. Uh but you
>> don't stereotype everybody. Uh but you know traditionally the 20-year-old who's
know traditionally the 20-year-old who's used crack cocaine probably doesn't have
used crack cocaine probably doesn't have athoscotic disease unless you get
athoscotic disease unless you get something out of their history in which
something out of their history in which case it's some homozygous or
case it's some homozygous or hetererozygous familial hyperpidemia
hetererozygous familial hyperpidemia situation. Um classic teaching on a
situation. Um classic teaching on a board exam is you know for board exams
board exam is you know for board exams is not to use beta blockers. Craig you
is not to use beta blockers. Craig you want to tell us why?
want to tell us why? >> Yeah. So I mean with the with the
>> Yeah. So I mean with the with the cocaine induced chest pain as you were
cocaine induced chest pain as you were mentioning it's a from the CNS and
mentioning it's a from the CNS and outflow of these catakolamines. So if
outflow of these catakolamines. So if you just block beta 1 and even beta 2
you just block beta 1 and even beta 2 you leave alpha essentially unopposed.
you leave alpha essentially unopposed. So since as you were mentioning this is
So since as you were mentioning this is a vasoc constrictive event you're going
a vasoc constrictive event you're going to certainly exacerbate that vasoc
to certainly exacerbate that vasoc constriction even further and actually
constriction even further and actually produce a legitimate uh mioardial
produce a legitimate uh mioardial eskemia or other eskeemia elsewhere. Um
eskemia or other eskeemia elsewhere. Um so you definitely don't want to do that.
so you definitely don't want to do that. Uh and again clinic in on a test it's
Uh and again clinic in on a test it's hard to perceive but clinically I mean
hard to perceive but clinically I mean we almost never give beta blocker versus
we almost never give beta blocker versus chest pain anyway. Um so it's not
chest pain anyway. Um so it's not something you would actually see in
something you would actually see in practice very commonly but on a test
practice very commonly but on a test question it would be something that you
question it would be something that you would have to rule out as a potential
would have to rule out as a potential answer. Yep. And why might you on the
answer. Yep. And why might you on the boards want to treat with a beta blocker
boards want to treat with a beta blocker in this case? And the answer is, I mean,
in this case? And the answer is, I mean, again, cocaine raises the pulse. And so
again, cocaine raises the pulse. And so some people might start going, well, the
some people might start going, well, the pulse is high. If I get the pulse down,
pulse is high. If I get the pulse down, I'm reducing the card oxygen demand.
I'm reducing the card oxygen demand. That's true, but you want to bring the
That's true, but you want to bring the pulse down by reducing the sympathetic
pulse down by reducing the sympathetic outflow and the tone,
outflow and the tone, >> right? So it's a it's you got to wrap
>> right? So it's a it's you got to wrap your mind around a little bit of the
your mind around a little bit of the approach that's slightly different than
approach that's slightly different than the traditional patient. Okay. Acute
the traditional patient. Okay. Acute limb eskeeia. So basically there's a
limb eskeeia. So basically there's a vascular event that's dropping reducing
vascular event that's dropping reducing uh usually arterial flow to a distal
uh usually arterial flow to a distal extremity most commonly the foot or leg.
extremity most commonly the foot or leg. And so they come in with excruciating
And so they come in with excruciating uh pain. They can have changes in the
uh pain. They can have changes in the the color of their uh skin. There's no
the color of their uh skin. There's no pulses. I mean you can look at it like
pulses. I mean you can look at it like oh there's something wrong here. You put
oh there's something wrong here. You put your hands on their skin. One's cool to
your hands on their skin. One's cool to touch. You can't feel a pulse. You get
touch. You can't feel a pulse. You get the Doppler. you can't hear it. That is
the Doppler. you can't hear it. That is an acute vascular occlusion until proven
an acute vascular occlusion until proven otherwise. Um you can if you have the
otherwise. Um you can if you have the ability and if you have access to the
ability and if you have access to the right cuffs uh you can do a ankle
right cuffs uh you can do a ankle brachial index. Basically, you do put a
brachial index. Basically, you do put a blood pressure cuff and measure the
blood pressure cuff and measure the systolic blood pressure and the from the
systolic blood pressure and the from the brachial artery and then you put a blood
brachial artery and then you put a blood pressure cuff on the around the low
pressure cuff on the around the low lower extremity and you check a
lower extremity and you check a basically around the uh uh the arteries
basically around the uh uh the arteries and the and the posterior tibial area or
and the and the posterior tibial area or dorsalis pedus and you basically are
dorsalis pedus and you basically are assessing blood flow through there
assessing blood flow through there usually using a Doppler. And so you do a
usually using a Doppler. And so you do a ratio and if it's less than 0.9 then
ratio and if it's less than 0.9 then something's oluding it. Okay? Because
something's oluding it. Okay? Because there's a significant drop in there. Um
there's a significant drop in there. Um most of the time if you're clinically
most of the time if you're clinically suspicious of this, this is considered
suspicious of this, this is considered an acute emergency. Uh usually they get
an acute emergency. Uh usually they get some sort of imaging study so that we we
some sort of imaging study so that we we will put in um you know we'll consult
will put in um you know we'll consult vascular surgery. Clearly they need to
vascular surgery. Clearly they need to be on board but in the meantime we put
be on board but in the meantime we put an IV in. We we take them to the CT
an IV in. We we take them to the CT scan, do a CT angio, look for the
scan, do a CT angio, look for the occlusion, you see it so that vascular
occlusion, you see it so that vascular surgery kind of knows where to go to
surgery kind of knows where to go to open that vessel back up. But it's
open that vessel back up. But it's anti-coagulation
anti-coagulation um and antiplatlet therapy and get that
um and antiplatlet therapy and get that stuff on board quickly and to
stuff on board quickly and to therapeutic levels as fast as you can.
therapeutic levels as fast as you can. Um and in the acute limb eskeemic
Um and in the acute limb eskeemic patient. Anything else there Craig?
patient. Anything else there Craig? >> Yeah, nothing critical to add here in my
>> Yeah, nothing critical to add here in my angle. All right. So, aneurismal disease
angle. All right. So, aneurismal disease basically the aneurysms uh when you have
basically the aneurysms uh when you have a area of the wall of a vessel that is
a area of the wall of a vessel that is weakened or some structural change has
weakened or some structural change has occurred and there's an outpouching
occurred and there's an outpouching essentially or it starts to dilate. Um
essentially or it starts to dilate. Um the triplea so uh abdominal aortic
the triplea so uh abdominal aortic aneurysm
aneurysm there are also ascending aortic
there are also ascending aortic aneurysms that are high up uh close to
aneurysms that are high up uh close to the heart. Those are very concerning um
the heart. Those are very concerning um can treated slightly a little different.
can treated slightly a little different. Uh AAA's are depending on their symptoms
Uh AAA's are depending on their symptoms and the size. Okay. So they can have
and the size. Okay. So they can have back pain because the aorta rests right
back pain because the aorta rests right on the inside the abdomen going down the
on the inside the abdomen going down the spine. So that many patients will come
spine. So that many patients will come in complaining of worsening uh
in complaining of worsening uh unexplained back pain with no trauma or
unexplained back pain with no trauma or injuries. that's an aneurysm or a
injuries. that's an aneurysm or a dissection until proven otherwise or
dissection until proven otherwise or epidural abscess if they have a fever.
epidural abscess if they have a fever. Okay? So, you have to think through what
Okay? So, you have to think through what else could be going on. But they're
else could be going on. But they're going to give you that information.
going to give you that information. Okay? They're going to give you the
Okay? They're going to give you the diagnosis. You're not going to be
diagnosis. You're not going to be expected to know that. But this a
expected to know that. But this a abdominal aortic aneurysm diameter,
abdominal aortic aneurysm diameter, which is most commonly and quickly
which is most commonly and quickly assessed at the bedside using a bedside
assessed at the bedside using a bedside ultrasound, typically when it's over
ultrasound, typically when it's over three and definitely when it's over
three and definitely when it's over five, is concerning. Now, as you age,
five, is concerning. Now, as you age, the vessel gets a little bit bigger
the vessel gets a little bit bigger because of athoscrotic disease. But once
because of athoscrotic disease. But once you start heading over that 3.5 and you
you start heading over that 3.5 and you get into that four to five window, those
get into that four to five window, those are the ones that can uh rupture on you.
are the ones that can uh rupture on you. And so you got to be very careful if
And so you got to be very careful if there's a high risk for rupture. uh you
there's a high risk for rupture. uh you want to bring down that pressure quickly
want to bring down that pressure quickly so that you don't open that vessel up
so that you don't open that vessel up because a large blood vessel like the
because a large blood vessel like the aorta you'll basically you know extinate
aorta you'll basically you know extinate inside and you can't stop that unless
inside and you can't stop that unless you surgically open them up and clamp
you surgically open them up and clamp off the aorta and then sew it up but you
off the aorta and then sew it up but you don't want to be doing that. You want to
don't want to be doing that. You want to be able to put in the graft you know in
be able to put in the graft you know in over or in around that um aneurysm to
over or in around that um aneurysm to avoid that. So the aortic dissections
avoid that. So the aortic dissections are different than a than a
are different than a than a um aneurysm in that there's a splitting
um aneurysm in that there's a splitting of the wall. So if you do a
of the wall. So if you do a cross-section of the blood vessel, you
cross-section of the blood vessel, you got a muscle around that uh aorta and
got a muscle around that uh aorta and basically there's a separation.
basically there's a separation. Okay, allowing blood to enter in through
Okay, allowing blood to enter in through that space ripping essentially and
that space ripping essentially and dissecting out uh flow. And we usually
dissecting out uh flow. And we usually see in these in hypertensive patients.
see in these in hypertensive patients. They come in with chest pain. So again,
They come in with chest pain. So again, it's kind of odd and you want to make
it's kind of odd and you want to make darn sure you don't have aortic
darn sure you don't have aortic dissection before you give somebody a
dissection before you give somebody a tpa drip, you know.
tpa drip, you know. >> Yeah.
>> Yeah. >> That that that will open it up and you
>> That that that will open it up and you will kill the patient and you will be
will kill the patient and you will be sued and that's the end of your career.
sued and that's the end of your career. Um and so do not mistaken that. But many
Um and so do not mistaken that. But many times they will describe the chest pain
times they will describe the chest pain as radiating to the back again because
as radiating to the back again because the aorta goes to back and around by the
the aorta goes to back and around by the spine and in between their shoulders.
spine and in between their shoulders. Um, and if this ruptures or leaks,
Um, and if this ruptures or leaks, you're dealing with cardiac arrest.
you're dealing with cardiac arrest. Usually, it's pea arrest.
Usually, it's pea arrest. >> Just three weeks ago, I had this exact
>> Just three weeks ago, I had this exact scenario.
scenario. Patient had sudden onset of severe back
Patient had sudden onset of severe back pain. Told the family members. She was
pain. Told the family members. She was like, "I don't know what's going on, but
like, "I don't know what's going on, but my pain is getting significantly worse,
my pain is getting significantly worse, and now I can't breathe." And she passed
and now I can't breathe." And she passed out. That was the end of it. She They
out. That was the end of it. She They came and unresponsive. Patient the
came and unresponsive. Patient the family picked her up, brought her in,
family picked her up, brought her in, but she was already cyanotic when she
but she was already cyanotic when she came in and we
came in and we >> I mean it was too late. She'd already
>> I mean it was too late. She'd already dissected and opened.
dissected and opened. >> Um but that's how it presents. So you
>> Um but that's how it presents. So you got to be in that case these patients
got to be in that case these patients are very very aggressive
are very very aggressive uh situation requires a a stat consult
uh situation requires a a stat consult to cardiothoracic surgery absolutely
to cardiothoracic surgery absolutely must be done first get them in there
must be done first get them in there because that's the only thing that's
because that's the only thing that's going to save this patient. Second is
going to save this patient. Second is from a pharmacologic treatment is you
from a pharmacologic treatment is you drop that pulse down to less than 60 as
drop that pulse down to less than 60 as fast as you can do it. And that's most
fast as you can do it. And that's most commonly going to be done with an esmal
commonly going to be done with an esmal drip. Most commonly you can use leol
drip. Most commonly you can use leol but most commonly you can titrate and
but most commonly you can titrate and control the pulse with an esmal drip and
control the pulse with an esmal drip and get it there the fastest and then you
get it there the fastest and then you give some something to reduce the
give some something to reduce the afterload so that you don't dissect that
afterload so that you don't dissect that wall further. And nitropide is the
wall further. And nitropide is the probably one of the more common uh
probably one of the more common uh agents used in that situation. But it is
agents used in that situation. But it is a rapid decline in the blood pressure or
a rapid decline in the blood pressure or systolic down to close to 100 and you
systolic down to close to 100 and you get that pulse to less than 60 and they
get that pulse to less than 60 and they go to cardiothoracic surgery as soon as
go to cardiothoracic surgery as soon as possible.
possible. >> Anything else to add here? Yeah, I would
>> Anything else to add here? Yeah, I would just uh echo the this definitely differs
just uh echo the this definitely differs from even though you would consider a
from even though you would consider a hypertensive emergency oftentimes when
hypertensive emergency oftentimes when we kind of talk about those conditions
we kind of talk about those conditions we say you have to lower the blood
we say you have to lower the blood pressure you know 25% and then a little
pressure you know 25% and then a little bit here or there over the next day
bit here or there over the next day aortic dissection is certainly an
aortic dissection is certainly an exclusion it's a hypertensive emergency
exclusion it's a hypertensive emergency but yeah so the the goal heart rate is
but yeah so the the goal heart rate is you immediately get to 60 immediately
you immediately get to 60 immediately and then a global blood pressure is 120
and then a global blood pressure is 120 systolic or less immediately. So it's
systolic or less immediately. So it's not you know a gradual
not you know a gradual >> you know.
>> you know. So again, you are absolutely bolising as
So again, you are absolutely bolising as malal uh absolutely the appropriate
malal uh absolutely the appropriate weight based dose like uh we've
weight based dose like uh we've mentioned in the past and then sodium
mentioned in the past and then sodium nitropide is is certainly an option as a
nitropide is is certainly an option as a a dilator because it it's more
a dilator because it it's more advantageous than nitroglycerin on its
advantageous than nitroglycerin on its own since nitropide does venus and
own since nitropide does venus and arterial dilation at a at the normal
arterial dilation at a at the normal dosing whereas nitroglycerin will only
dosing whereas nitroglycerin will only do venus dilation at your typical
do venus dilation at your typical dosing. Um, so you'd have to be giving
dosing. Um, so you'd have to be giving much much higher doses on the order of
much much higher doses on the order of like two to 400 mics per mics per
like two to 400 mics per mics per minute. Um, which isn't going to be
minute. Um, which isn't going to be started. Um, so you're actually going to
started. Um, so you're actually going to make it worse if you give nitroglycerin
make it worse if you give nitroglycerin first. So nitropide would be the
first. So nitropide would be the appropriate one here.
appropriate one here. >> Yeah. And just so you guys know, the
>> Yeah. And just so you guys know, the order if they ask you the question, it
order if they ask you the question, it is the reducing the pulse first,
is the reducing the pulse first, >> right?
>> right? >> Because you don't want to dilate them
>> Because you don't want to dilate them and cause reflex tacocardia which can
and cause reflex tacocardia which can actually increase shear forces and
actually increase shear forces and dissect them out further. So you drop
dissect them out further. So you drop the pulse first. First you start the
the pulse first. First you start the esmalol first and then you do some basil
esmalol first and then you do some basil dilator second. Um and that's why people
dilator second. Um and that's why people sometimes will go to ledol because
sometimes will go to ledol because they're hitting both at basically the
they're hitting both at basically the same time. But but to get it there
same time. But but to get it there quickly
quickly uh clinically uh if you see esmalol with
uh clinically uh if you see esmalol with nitroide that is the answer.
nitroide that is the answer. >> Yeah. And again, one one super quick
>> Yeah. And again, one one super quick thing. I know you were mentioning the
thing. I know you were mentioning the aortic dissection when you were kind of
aortic dissection when you were kind of de or demonstrating that, but again, if
de or demonstrating that, but again, if you're an emergency medicine, you can
you're an emergency medicine, you can sit by an ultrasound. You can see the
sit by an ultrasound. You can see the Pepsi sign, which you know, identically
Pepsi sign, which you know, identically describes exactly what you were talking
describes exactly what you were talking about. So, you know, the Pepsi logo,
about. So, you know, the Pepsi logo, it's a circle with a line in the middle.
it's a circle with a line in the middle. That's exactly what the order looks like
That's exactly what the order looks like uh if it's dissected.
uh if it's dissected. >> Yep. Yep. And they're sweating and
>> Yep. Yep. And they're sweating and you're starting to sweat. All right.
you're starting to sweat. All right. Aortic stenosis. Basically this is an
Aortic stenosis. Basically this is an outflow obstruction from the aortic
outflow obstruction from the aortic valve. So remember the left ventricle
valve. So remember the left ventricle contracts. It pushes the blood out of
contracts. It pushes the blood out of the uh left ventricle into the aorta
the uh left ventricle into the aorta through the aortic valve. If that valve
through the aortic valve. If that valve is stenotic uh then basically it's rigid
is stenotic uh then basically it's rigid or the valve doesn't open and there's
or the valve doesn't open and there's just a little hole. So the blood is like
just a little hole. So the blood is like spraying through there literally. Um and
spraying through there literally. Um and these this can cause a number of
these this can cause a number of symptoms. Uh especially if there's a
symptoms. Uh especially if there's a drop in preload all of a sudden uh they
drop in preload all of a sudden uh they can become very orthostatic and
can become very orthostatic and lightaded dizzy. Um and also what
lightaded dizzy. Um and also what happens just distal to the aortic valve
happens just distal to the aortic valve is the opening to the coronaries. So you
is the opening to the coronaries. So you can actually cause uh chest discomfort
can actually cause uh chest discomfort in these patients. So you want to be
in these patients. So you want to be very very careful at um sudden changes
very very careful at um sudden changes in blood pressures and preload in these
in blood pressures and preload in these patients. Um now on exam what you'll
patients. Um now on exam what you'll classically hear is a uh systolic
classically hear is a uh systolic murmur. Many times it will radiate up
murmur. Many times it will radiate up into the corateed. Again, it's just
into the corateed. Again, it's just something that may show up on the boards
something that may show up on the boards that you'll hear or in the descriptor
that you'll hear or in the descriptor because your blueprint still does talk
because your blueprint still does talk about fact the fact you need to know
about fact the fact you need to know clinical signs and symptoms and
clinical signs and symptoms and presentation, which is why we're going
presentation, which is why we're going over this stuff. So, there are different
over this stuff. So, there are different grades of aortic stenosis based on the
grades of aortic stenosis based on the the um flow rate or the volume of blood
the um flow rate or the volume of blood that can pass by.
that can pass by. Um, so they need an ultrasound to uh or
Um, so they need an ultrasound to uh or a cardiac echo, sorry, uh to help you to
a cardiac echo, sorry, uh to help you to discern that. Um, but what you want to
discern that. Um, but what you want to be very careful of in these patients,
be very careful of in these patients, especially if they have underlying
especially if they have underlying hypertension, which many times they do,
hypertension, which many times they do, you do not want to be aggressive with
you do not want to be aggressive with their anti-hypertensive medication too
their anti-hypertensive medication too quickly. Uh, you don't want to titose or
quickly. Uh, you don't want to titose or titrate too fast because those are the
titrate too fast because those are the patients where you drop their preload
patients where you drop their preload and have load and they become very
and have load and they become very orthostite. They can syncopize on you uh
orthostite. They can syncopize on you uh very easily. So be very very careful in
very easily. So be very very careful in those patients. All right. Atrial
those patients. All right. Atrial fibrillation. The first one that we're
fibrillation. The first one that we're going to talk about is chronic and then
going to talk about is chronic and then we'll mention uh the acute situation. So
we'll mention uh the acute situation. So basically you have the atria the two
basically you have the atria the two chambers on top that are fibrillating
chambers on top that are fibrillating and I'll just tell you that most atria
and I'll just tell you that most atria fibrillate around 300 beats there 300
fibrillate around 300 beats there 300 beats in there if you were to map them
beats in there if you were to map them all out. Okay, we don't see 300 beats or
all out. Okay, we don't see 300 beats or pulse because you got traditionally the
pulse because you got traditionally the AV node controlling it, right? So it's
AV node controlling it, right? So it's blocking that uh those fibrillations
blocking that uh those fibrillations from entering into the ventricle. Um but
from entering into the ventricle. Um but there's clearly multifi happening in the
there's clearly multifi happening in the atrium that is stimulating that heart
atrium that is stimulating that heart rate to do to to do that. Well, you
rate to do to to do that. Well, you don't get adequate forward movement of
don't get adequate forward movement of the flow. So basically uh you don't get
the flow. So basically uh you don't get atrial kick, you don't get that forward
atrial kick, you don't get that forward movement and so patients can start
movement and so patients can start having uh backing up especially from the
having uh backing up especially from the left side to the right side and then
left side to the right side and then obviously they can back up into the
obviously they can back up into the lungs and also into the periphery
lungs and also into the periphery basically put them in a heart failure.
basically put them in a heart failure. Uh many times atrial fibrillation is
Uh many times atrial fibrillation is what exacerbates heart failure u because
what exacerbates heart failure u because you don't get that good forward flow.
you don't get that good forward flow. Okay. Um so basically it's a diagnosed
Okay. Um so basically it's a diagnosed by exam. So you feel their pulse and you
by exam. So you feel their pulse and you can listen to it. It's irregularly
can listen to it. It's irregularly irregular. Okay? So it's not, you know,
irregular. Okay? So it's not, you know, love dub love dub. It's all all these
love dub love dub. It's all all these weird beats that don't make any sense.
weird beats that don't make any sense. And you might feel half of them and you
And you might feel half of them and you might not feel the other half, right?
might not feel the other half, right? When you're hearing it. Um and and
When you're hearing it. Um and and certainly the EKG. Now for for control,
certainly the EKG. Now for for control, all right, uh most of the time it's rate
all right, uh most of the time it's rate control. And many times these patients
control. And many times these patients might need something for rate control
might need something for rate control whether it's like a dyropodian calcium
whether it's like a dyropodian calcium channel blocker or or a beta blocker um
channel blocker or or a beta blocker um can do that to offer them control. The
can do that to offer them control. The kicker is if they have you always want
kicker is if they have you always want to rule this out on the boards is don't
to rule this out on the boards is don't traditionally give non-dyropertian
traditionally give non-dyropertian calcium channel blockers delta and rap
calcium channel blockers delta and rap to patients with a history of WPW which
to patients with a history of WPW which is with Parkinson's white syndrome
is with Parkinson's white syndrome because they have an accessory pathway
because they have an accessory pathway that theoretically can be worsened uh if
that theoretically can be worsened uh if you would do that. Um and that's
you would do that. Um and that's probably what they might ask you. Craig,
probably what they might ask you. Craig, anything else on here?
anything else on here? >> No, I mean I think it's a good coverage.
>> No, I mean I think it's a good coverage. There's there's a lot to debate too
There's there's a lot to debate too here. It could be a whole separate
here. It could be a whole separate lecture. But I think this is a good good
lecture. But I think this is a good good >> for the last the last thing to to
>> for the last the last thing to to consider here is uh not just management
consider here is uh not just management of the dysriythmia but also the
of the dysriythmia but also the prevention of the complications and
prevention of the complications and that's where the Chad's vast who you
that's where the Chad's vast who you know scores can be helpful at predicting
know scores can be helpful at predicting the risk of poor outcomes and the risk
the risk of poor outcomes and the risk of bleeding. And so what is the risk of
of bleeding. And so what is the risk of cardioic stroke? And then you compare
cardioic stroke? And then you compare that to obviously the risk of of
that to obviously the risk of of bleeding. So the anti-coagulants have a
bleeding. So the anti-coagulants have a certain level of bleeding that is that
certain level of bleeding that is that are likely there. And when that risk of
are likely there. And when that risk of cardio stroke uh is higher than the risk
cardio stroke uh is higher than the risk of bleeding then then it warrants
of bleeding then then it warrants initiation. You don't need to know the
initiation. You don't need to know the actual risk stratification tool like how
actual risk stratification tool like how to calculate it, what are all the
to calculate it, what are all the variables and how to generate the
variables and how to generate the number. They're going to give you those
number. They're going to give you those parameters and guide you. Um and then if
parameters and guide you. Um and then if there's a you know like has blood can be
there's a you know like has blood can be used if patients have underlying um you
used if patients have underlying um you know risk for bleeding. So you're trying
know risk for bleeding. So you're trying to weigh all these things out but just
to weigh all these things out but just recognize these are risk stratification
recognize these are risk stratification tools that do have some degree of
tools that do have some degree of validation in clinical trials but
validation in clinical trials but they're also not perfect. Um Craig I
they're also not perfect. Um Craig I don't know if there's anything else you
don't know if there's anything else you want to add there.
want to add there. >> No.
>> No. >> Yeah. So rhythm control Miranda would
>> Yeah. So rhythm control Miranda would only be added if there had been a
only be added if there had been a history of RVR.
history of RVR. Um so that's leads us to this question.
Um so that's leads us to this question. So you now have the atrial fibrillation.
So you now have the atrial fibrillation. Now it's passing through into the
Now it's passing through into the ventricles and the ventricles are
ventricles and the ventricles are responding and uh when that happens it's
responding and uh when that happens it's usually half. So it's like a 2 to one.
usually half. So it's like a 2 to one. So if your atria is beaten at 300
So if your atria is beaten at 300 roughly and half of them make it in then
roughly and half of them make it in then you you commonly see an AIB with RVR
you you commonly see an AIB with RVR about a 150 beats per minute. That's the
about a 150 beats per minute. That's the classic. And then of course you do the
classic. And then of course you do the EKG you can see that versus a flutter
EKG you can see that versus a flutter has a saw to pattern. Um and it can have
has a saw to pattern. Um and it can have different you know two to one 3 to one
different you know two to one 3 to one depending on what pattern you see.
depending on what pattern you see. >> Um but these patients can obviously with
>> Um but these patients can obviously with increased pulse get are still not
increased pulse get are still not getting good forward flow and if they
getting good forward flow and if they have underlying heart disease which many
have underlying heart disease which many times they do
times they do um then you want to they'll probably go
um then you want to they'll probably go into heart failure. So you gota slow
into heart failure. So you gota slow down that rate because you're increasing
down that rate because you're increasing their oxygen demand which can then put
their oxygen demand which can then put them into a cardiac uh um heart attack
them into a cardiac uh um heart attack or another dysriythmia as well. So in
or another dysriythmia as well. So in this case they you want to uh rate
this case they you want to uh rate control them if they're hemodynamically
control them if they're hemodynamically stable. Um what should you use deltaism
stable. Um what should you use deltaism you know
you know which one? Well, I clinically um and I
which one? Well, I clinically um and I think for the boards it would be the
think for the boards it would be the same thing too is use the one that they
same thing too is use the one that they were on. So if they had chronically were
were on. So if they had chronically were on a beta blocker then that you know
on a beta blocker then that you know they can handle the beta blocker give
they can handle the beta blocker give them a dose of their beta blocker or
them a dose of their beta blocker or give them a beta blocker like lebalol IV
give them a beta blocker like lebalol IV or something. Um but if you don't have
or something. Um but if you don't have any history and they're coming in with
any history and they're coming in with acute onset and first time diagnosis
acute onset and first time diagnosis then the most classic answer is delta
then the most classic answer is delta tism unless it's WPW then it would be
tism unless it's WPW then it would be mtopra or procanomite Craig anything you
mtopra or procanomite Craig anything you want to add to that
want to add to that uh no I mean I I would certainly agree
uh no I mean I I would certainly agree with that uh knowing their medical
with that uh knowing their medical history and the medicine history that
history and the medicine history that that's something that actually got
that's something that actually got brought up uh in my own practice making
brought up uh in my own practice making sure they're on what they're on, you're
sure they're on what they're on, you're actually giving them um because
actually giving them um because compliance just might be an issue either
compliance just might be an issue either in the RVR. So, we can just, you know,
in the RVR. So, we can just, you know, yeah, kind of supplement that. But, um
yeah, kind of supplement that. But, um you definitely don't want to have kind
you definitely don't want to have kind of a I don't I don't want to say this in
of a I don't I don't want to say this in a positive sense, but a compliment
a positive sense, but a compliment complimentary AV block. That could
complimentary AV block. That could potentially make things even worse if
potentially make things even worse if you go down the wrong route. Um but
you go down the wrong route. Um but yeah, so definitely definitely within
yeah, so definitely definitely within reason. So if they if they give you a
reason. So if they if they give you a with RVR with WPW and you give dilism
with RVR with WPW and you give dilism and breath mill then they're probably
and breath mill then they're probably concerned that you're going to worsen
concerned that you're going to worsen the pulse. So don't give it. Okay. If
the pulse. So don't give it. Okay. If you see procanomide that's definitely an
you see procanomide that's definitely an option. If you if you don't see
option. If you if you don't see procanomide beta blocker okay
>> Yeah, turopaab bandan. They're they're commonly used nowadays. So if you at a
commonly used nowadays. So if you at a place as you were mentioning earlier, if
place as you were mentioning earlier, if you're at a hospital that does a GPTB3A
you're at a hospital that does a GPTB3A plus hepin, that's what they use. Or
plus hepin, that's what they use. Or you're at a institution that does
you're at a institution that does balrudin that's what they use. It it
balrudin that's what they use. It it just depends uh the cardiology group or
just depends uh the cardiology group or what determination they want. I practice
what determination they want. I practice at places that does one then it moves
at places that does one then it moves somewhere else to this but they do the
somewhere else to this but they do the other and there's no differentiation but
other and there's no differentiation but and Amanda just so you know too if uh
and Amanda just so you know too if uh and this is a she you bring up a great
and this is a she you bring up a great question uh but for everybody else me so
question uh but for everybody else me so remember the glyoprotein 2B3 receptor
remember the glyoprotein 2B3 receptor blockers are largely re reserved for the
blockers are largely re reserved for the STEMI patient
STEMI patient >> not in STEMI that that would be a trick
>> not in STEMI that that would be a trick on the boards
on the boards >> so if they give you the clear diagnosis
>> so if they give you the clear diagnosis of NT STEMI you're not using tpa and
of NT STEMI you're not using tpa and you're not using glyoprotein 2b3
you're not using glyoprotein 2b3 receptor blockers just don't go there.
receptor blockers just don't go there. >> Now do we start uh if they're if they
>> Now do we start uh if they're if they are clearly known and there's strong
are clearly known and there's strong suspicion that they need to go to the
suspicion that they need to go to the kath lab
kath lab um the um
um the um then you might help the cardiologist by
then you might help the cardiologist by because they're going to need if they if
because they're going to need if they if they stent the patient
they stent the patient they're going to need something.
they're going to need something. >> Yeah. And so, but usually the Kath Lab
>> Yeah. And so, but usually the Kath Lab team is the one starting all that stuff.
team is the one starting all that stuff. >> Okay.
>> Okay. >> Not not not not us in a department or or
>> Not not not not us in a department or or you know where we traditionally start
you know where we traditionally start some of these medications. But I've been
some of these medications. But I've been in scenarios where I've been asked to go
in scenarios where I've been asked to go ahead and start something or the
ahead and start something or the cardiologist depending on the EKG or you
cardiologist depending on the EKG or you know or the history wants us to do that.
know or the history wants us to do that. Um but that would not probably show up
Um but that would not probably show up on a board exam ever.
on a board exam ever. Uh so
Uh so could you please repeat what medications
could you please repeat what medications we'll be able to use in patient with
we'll be able to use in patient with aphib? All right. So if you have ahib
aphib? All right. So if you have ahib with RVR and the patient has WPW
with RVR and the patient has WPW with Parkinson's white syndrome, you do
with Parkinson's white syndrome, you do not want to use traditional AVO blocking
not want to use traditional AVO blocking drugs like dilism and verapamil.
drugs like dilism and verapamil. In those cases, you want to um consider
In those cases, you want to um consider um other drugs that would slow the heart
um other drugs that would slow the heart rate or nodal cells. Um
rate or nodal cells. Um and so you can consider drugs like
and so you can consider drugs like amorone and or beta blockers or if
amorone and or beta blockers or if you're in the acute scenario where the
you're in the acute scenario where the boards are probably going to go is there
boards are probably going to go is there you'll probably see procanamite on
you'll probably see procanamite on there.
there. >> Yeah. It it's just traditional teaching
>> Yeah. It it's just traditional teaching >> although the availability of procanomide
>> although the availability of procanomide is
is >> somewhat
>> somewhat difficult. So if you don't so on board
difficult. So if you don't so on board exam yes clinically it isn't always
exam yes clinically it isn't always available especially if you're in a
available especially if you're in a community environment that doesn't stock
community environment that doesn't stock that kind of crap. Uh not that it's
that kind of crap. Uh not that it's crap. I mean it's it's got its use.
crap. I mean it's it's got its use. Sorry I didn't mean to say that that
Sorry I didn't mean to say that that way. All right. So we had a question
way. All right. So we had a question here. Thanks for the lecture regarding
here. Thanks for the lecture regarding statistics statistics. Can BPS ask you a
statistics statistics. Can BPS ask you a question that requires us to
question that requires us to differentiate the correct statistical
differentiate the correct statistical analysis for a study? Absolutely.
analysis for a study? Absolutely. They're going to give you the study
They're going to give you the study methodology.
methodology. >> Yeah.
>> Yeah. >> First though, they're not going to say
>> First though, they're not going to say on the Rails trial, what statistical
on the Rails trial, what statistical test was used,
test was used, >> right?
>> right? >> That is not a test question. Um and if
>> That is not a test question. Um and if they ever do that, they would not do
they ever do that, they would not do that. They're not that stupid.
that. They're not that stupid. >> They're not going to do that. For
>> They're not going to do that. For example, the question gives you two
example, the question gives you two independent samples and the data is
independent samples and the data is nominal, but the answer choice is either
nominal, but the answer choice is either a kai square. Absolutely. That's a very
a kai square. Absolutely. That's a very legitimate question 100%.
legitimate question 100%. >> Yep.
>> Yep. >> You need to now know why do you pick a
>> You need to now know why do you pick a kai squared over a fisher exact. You
kai squared over a fisher exact. You need to listen to my lecture.
need to listen to my lecture. >> I would agree.
>> I would agree. >> I answer all that stuff for you, bro.
>> I answer all that stuff for you, bro. >> I would agree. That's definitely
>> I would agree. That's definitely testable. Uh, if I pass, can I get a
testable. Uh, if I pass, can I get a sweater? You like our You like the over
sweater? You like our You like the over the the throw here, bro?
the the throw here, bro? >> Betsy.
>> Talk to me when you pass. >> Talk to me when you pass. We got some
>> Talk to me when you pass. We got some cool We got some cool uh
cool We got some cool uh >> true
>> true >> clothes.
>> clothes. >> I'm serious. Have you seen our t-shirts?
>> I'm serious. Have you seen our t-shirts? >> I got that on, too.
>> I got that on, too. Hey, the t-shirt, the best t-shirt on
Hey, the t-shirt, the best t-shirt on the planet
the planet is my sonic crew P450 is faster than
is my sonic crew P450 is faster than yours.
>> That's true. >> It's good.
>> It's good. >> All right.
>> All right. Oh, you have the high I'm high yield.
Oh, you have the high I'm high yield. You are, Amanda. I believe that you are
You are, Amanda. I believe that you are high yield. You're definitely high yield
high yield. You're definitely high yield webinar.
webinar. >> That's for sure. All right. Uh let's
>> That's for sure. All right. Uh let's see. Jennifer says, "Uh, would it uh
see. Jennifer says, "Uh, would it uh would it be good to know which drugs
would it be good to know which drugs cannot be given
cannot be given through the same IV line such as a tiff
through the same IV line such as a tiff of a tide and no, I do not see that
of a tide and no, I do not see that being a board question. I've never
being a board question. I've never >> I agree.
>> I agree. >> Never seen that uh type of question
>> Never seen that uh type of question asked, but it's a good you're asking a
asked, but it's a good you're asking a good question. Excellent question,
good question. Excellent question, Jennifer. I don't never think that will
Jennifer. I don't never think that will ever make it to a board exam." I would
ever make it to a board exam." I would agree.
agree. >> All right, guys. We finished.
>> All right, guys. We finished. >> All right. All right. Well, I'm assuming
>> All right. All right. Well, I'm assuming there's no more questions. Uh outside of
there's no more questions. Uh outside of that, we will see you guys next time.
that, we will see you guys next time. Keep it fun.
Keep it fun. Be good. Take care of your patients. Be
Be good. Take care of your patients. Be awesome like you are. Take care. Bye.
awesome like you are. Take care. Bye. Have a good one.
Click on any text or timestamp to jump to that moment in the video
Share:
Most transcripts ready in under 5 seconds
One-Click Copy125+ LanguagesSearch ContentJump to Timestamps
Paste YouTube URL
Enter any YouTube video link to get the full transcript
Transcript Extraction Form
Most transcripts ready in under 5 seconds
Get Our Chrome Extension
Get transcripts instantly without leaving YouTube. Install our Chrome extension for one-click access to any video's transcript directly on the watch page.