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Session 2 - Live Rapid Review for BPS Exams

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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.

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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

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 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

procanomide beta blocker okay >> uh that's classic teaching. All right.

>> uh that's classic teaching. All right. If you have a with RVR no WPW no prior

If you have a with RVR no WPW no prior use you just go ahead and give Dilt.

use you just go ahead and give Dilt. Okay. Uh, is Dilt gonna offer remodeling

Okay. Uh, is Dilt gonna offer remodeling effects? No. Right? But that's not what

effects? No. Right? But that's not what you're trying to do here. You're trying

you're trying to do here. You're trying to get them rate controlled and then you

to get them rate controlled and then you can figure out the problem. And

can figure out the problem. And sometimes it's just that they were in a

sometimes it's just that they were in a heart failure exacerbation. So, as we

heart failure exacerbation. So, as we talk about heart failure, there's

talk about heart failure, there's multiple types of heart failure. Um and

multiple types of heart failure. Um and this is the acute decompensated

this is the acute decompensated heart failure where basically you lack

heart failure where basically you lack appropriate cardiac output because their

appropriate cardiac output because their stroke volume has been compromised

stroke volume has been compromised because usually inotropic support has

because usually inotropic support has been affected and this is usually from

been affected and this is usually from left ventricular systolic dysfunction in

left ventricular systolic dysfunction in most cases. Okay, not 100% but in most

most cases. Okay, not 100% but in most cases and so you decrease cardiac

cases and so you decrease cardiac output. Well, you decrease profusion to

output. Well, you decrease profusion to the brain, you decrease profusion to the

the brain, you decrease profusion to the kidneys, kidneys start ramping up RAS,

kidneys, kidneys start ramping up RAS, you just have this cycling and it

you just have this cycling and it usually results in fluid overload. These

usually results in fluid overload. These patients many time in the acute phase

patients many time in the acute phase come in with a pulmonary edema that that

come in with a pulmonary edema that that you can hear in the lungs on a lung exam

you can hear in the lungs on a lung exam crackles. Uh they're short of breath.

crackles. Uh they're short of breath. They can have JVD if especially when

They can have JVD if especially when they have right side heart failure. And

they have right side heart failure. And then obviously lower extremity edema

then obviously lower extremity edema that can be from you know just the

that can be from you know just the calves all the way up to the thigh or

calves all the way up to the thigh or even be anarchic. Okay, which is

even be anarchic. Okay, which is basically all over themselves. U and

basically all over themselves. U and their weights are are high. And so in

their weights are are high. And so in these situations uh patients may need

these situations uh patients may need acute control before they decompensate

acute control before they decompensate further. Again heart failure people the

further. Again heart failure people the reason they die of of sudden cardiac

reason they die of of sudden cardiac death is they go into ventricular uh

death is they go into ventricular uh dysriythmia like VTAC or VIP which we've

dysriythmia like VTAC or VIP which we've already discussed. So you don't want

already discussed. So you don't want them doing that. Okay. So how do you

them doing that. Okay. So how do you kind of correct this quickly if they

kind of correct this quickly if they have pulmonary edema shortness of breath

have pulmonary edema shortness of breath and they're not getting good forward

and they're not getting good forward flow? Well, you can't just make the

flow? Well, you can't just make the volume go away instantaneously.

volume go away instantaneously. So, you try to reduce that uh acutely.

So, you try to reduce that uh acutely. You try to reduce the preload and the

You try to reduce the preload and the vascular congestion. You try to reduce

vascular congestion. You try to reduce the preload and the afterload so that

the preload and the afterload so that you encourage some forward flow. So a

you encourage some forward flow. So a vasoddilator nitroglycerin is very

vasoddilator nitroglycerin is very effective and plus or minus a positive

effective and plus or minus a positive pressure ventilation which is basically

pressure ventilation which is basically like a byp machine that opens up the

like a byp machine that opens up the airway the distal airways and the alvei

airway the distal airways and the alvei and starts pushing that fluid out of

and starts pushing that fluid out of their lungs.

their lungs. As you reduce the preload and afterload,

As you reduce the preload and afterload, you start to recalibrate the hemodynamic

you start to recalibrate the hemodynamic forward flow. And within 15 or 20

forward flow. And within 15 or 20 minutes of doing that with sublingual

minutes of doing that with sublingual nitric, many times you can get them off

nitric, many times you can get them off the biap and they start feeling a little

the biap and they start feeling a little bit better. Yeah, of course you're

bit better. Yeah, of course you're giving them a loop diuretic IV, not PO

giving them a loop diuretic IV, not PO because you don't want to impact. You

because you don't want to impact. You want 100% bioavailability so you

want 100% bioavailability so you maximize the drug delivery to the

maximize the drug delivery to the kidneys so you can start to diarase the

kidneys so you can start to diarase the patient. And then then you start seeing

patient. And then then you start seeing them improve. If they're hypotensive and

them improve. If they're hypotensive and not responding, which means now you

not responding, which means now you can't give nitroglycerin if they're

can't give nitroglycerin if they're hypotensive. Now you're stuck. Okay?

hypotensive. Now you're stuck. Okay? Because if you increase thoracic

Because if you increase thoracic pressure too much with BiPAP or CPAP,

pressure too much with BiPAP or CPAP, you're reducing preload.

you're reducing preload. Well, you might tank them further. So

Well, you might tank them further. So this is a very delicate. Well, now we're

this is a very delicate. Well, now we're stepping into critical care. Uh, I mean

stepping into critical care. Uh, I mean this is a no every decision you do has a

this is a no every decision you do has a double-edged sword to it. So you start

double-edged sword to it. So you start thinking I got to give an inotrope. So

thinking I got to give an inotrope. So you know do you give dobutamine,

you know do you give dobutamine, dopamine, right? Those kind of drugs,

dopamine, right? Those kind of drugs, milone,

milone, especially if they're already beta

especially if they're already beta blocked. That's where you're starting to

blocked. That's where you're starting to think in that direction. And it's just

think in that direction. And it's just not easy. Some people may even need

not easy. Some people may even need diialysis to get the fluid off under a

diialysis to get the fluid off under a delicate situation. It's very there's

delicate situation. It's very there's more than one way to do it.

more than one way to do it. >> Uh so it's no oneizefits-all, but you

>> Uh so it's no oneizefits-all, but you have to start thinking that way. Okay.

have to start thinking that way. Okay. So that's acute. Anything else to add

So that's acute. Anything else to add there?

there? >> Uh I would just echo what we were

>> Uh I would just echo what we were mentioning in the in the previous topic

mentioning in the in the previous topic where if a patient's on a beta blocker

where if a patient's on a beta blocker for their chronic heart failure come in

for their chronic heart failure come in with ADHD, do may not be the best

with ADHD, do may not be the best option. So, Milrenone might be a good

option. So, Milrenone might be a good substitute here since again they work on

substitute here since again they work on different pathways. Um, that's that's

different pathways. Um, that's that's one thing to consider. Um, I think

one thing to consider. Um, I think there's a lot of other context uh kind

there's a lot of other context uh kind of discussions that we could go on here

of discussions that we could go on here on a lot of different tangents too. But,

on a lot of different tangents too. But, um, I think that that's one again

um, I think that that's one again highdose dopamine, not your, you know,

highdose dopamine, not your, you know, low renal dosing dopamine. I know that

low renal dosing dopamine. I know that came up the other day, too, but we want

came up the other day, too, but we want to make sure it's high dose to

to make sure it's high dose to appropriately manage this.

appropriately manage this. >> All right. And heart failure with

>> All right. And heart failure with preserved EF. So this is not necessarily

preserved EF. So this is not necessarily left ventricular systolic dysfunction

left ventricular systolic dysfunction fully yet. So they're have some

fully yet. So they're have some functional capacity there where they're

functional capacity there where they're able to get some stroke volume. So at

able to get some stroke volume. So at this point you're really trying to you

this point you're really trying to you can still have these symptoms and people

can still have these symptoms and people can have an acute and then once you get

can have an acute and then once you get rid of the fluid can start to normalize

rid of the fluid can start to normalize some of their symptoms and even improve

some of their symptoms and even improve their EF. And so at this point, you want

their EF. And so at this point, you want to go down the traditional chronic

to go down the traditional chronic pathway where you're thinking of stage

pathway where you're thinking of stage A, B, C, D, and treatments, right? They

A, B, C, D, and treatments, right? They might present in stage C, the acute

might present in stage C, the acute side, but what is their baseline once

side, but what is their baseline once you once you get rid of that fluid? Um,

you once you get rid of that fluid? Um, and so when you think about first-line

and so when you think about first-line treatments in stage A, ACE inhibitors or

treatments in stage A, ACE inhibitors or an ARB, okay, followed by beta blockers

an ARB, okay, followed by beta blockers because both of those drugs in

because both of those drugs in particular are going to have uh

particular are going to have uh mortality benefits but also remodeling

mortality benefits but also remodeling benefits. And of the beta blockers, it's

benefits. And of the beta blockers, it's your mtopol suinate and carvdalol. Um,

your mtopol suinate and carvdalol. Um, and then obviously sacubitrol with uh um

and then obviously sacubitrol with uh um valartin,

valartin, right? So that one's also another one

right? So that one's also another one that's been introduced in the past

that's been introduced in the past several years into the treatment. So

several years into the treatment. So those are like your very early on and

those are like your very early on and then treating underlying problems of

then treating underlying problems of making sure they're on aspirin, treating

making sure they're on aspirin, treating their dispeia, all that other stuff.

their dispeia, all that other stuff. Sure, you got to definitely do that. But

Sure, you got to definitely do that. But those are the key drugs because of their

those are the key drugs because of their mortality benefits. And you said you see

mortality benefits. And you said you see there the addition of eldoststerone

there the addition of eldoststerone antagonist really comes from the Rails

antagonist really comes from the Rails trial and the Ephesus trial. Rails trial

trial and the Ephesus trial. Rails trial was stopped early because the mortality

was stopped early because the mortality benefit was so profound in these

benefit was so profound in these patients that it was unethical to

patients that it was unethical to continue the study. Ephesus wasn't

continue the study. Ephesus wasn't stopped

stopped um like like rails was. But so you

um like like rails was. But so you consider those treatments that obviously

consider those treatments that obviously give the mortality benefits first and as

give the mortality benefits first and as much as possible. U anything else to add

much as possible. U anything else to add there?

there? >> No, I think that was good.

>> No, I think that was good. >> Yeah. And that's why you don't see dig

>> Yeah. And that's why you don't see dig on there by the way. So dig is one of

on there by the way. So dig is one of those adjuncts that you would consider

those adjuncts that you would consider when you're in stage C, you know, after

when you're in stage C, you know, after you've tried all those other agents.

you've tried all those other agents. All right, reduced heart f or reduced

All right, reduced heart f or reduced EF. So the EF ejection faction is less

EF. So the EF ejection faction is less than uh 40, you still consider these

than uh 40, you still consider these things, but now they're probably on loop

things, but now they're probably on loop diuretics for sure. So when we see

diuretics for sure. So when we see diuretics over here, if they're in stage

diuretics over here, if they're in stage A B, it might be just the thyide. But

A B, it might be just the thyide. But once you hit the stage C level, they're

once you hit the stage C level, they're probably having fluid problems and

probably having fluid problems and that's where the combination of loop

that's where the combination of loop diuretics with aldoststerone antagonists

diuretics with aldoststerone antagonists are being used. Just keep in mind that

are being used. Just keep in mind that aldoststerone antagonists are

aldoststerone antagonists are problematic because you're also using

problematic because you're also using them in the context of an ACE inhibitor

them in the context of an ACE inhibitor or an ARB. So you start getting into

or an ARB. So you start getting into this issue with your um potassium

this issue with your um potassium levels um especially if somebody is

levels um especially if somebody is using salt substitute. So just these are

using salt substitute. So just these are like the little nuances that just want

like the little nuances that just want to make sure you hit those key points.

to make sure you hit those key points. All right. Hokum. So this is an outflow

All right. Hokum. So this is an outflow obstruction basically uh that's dynamic.

obstruction basically uh that's dynamic. So the stronger their theirotropic force

So the stronger their theirotropic force the actually the greater the obstruction

the actually the greater the obstruction of movement of the blood out so the

of movement of the blood out so the stroke volume drops. Uh we can many

stroke volume drops. Uh we can many times see these in younger patients who

times see these in younger patients who have these hypertrophic cardiomyopathies

have these hypertrophic cardiomyopathies basically enlarged heart lots of muscle

basically enlarged heart lots of muscle but it's in the septum and it's right up

but it's in the septum and it's right up by the uh valve

by the uh valve and so basically what ends up happening

and so basically what ends up happening is it it it bows and it prevents the

is it it it bows and it prevents the blood from escaping properly and so they

blood from escaping properly and so they can basically pass out um and they can

can basically pass out um and they can go into sard sudden cardiac uh death as

go into sard sudden cardiac uh death as a result of that. That's why you've seen

a result of that. That's why you've seen like sports players and these have they

like sports players and these have they sometimes will get EKGs to rule out or

sometimes will get EKGs to rule out or get screened for hokum because no one

get screened for hokum because no one wants to have some kid on the court or

wants to have some kid on the court or on the field you know pass out because

on the field you know pass out because of undiagnosed hokum and there's been

of undiagnosed hokum and there's been clearly a number of cases um where

clearly a number of cases um where that's happened. So when you look at

that's happened. So when you look at bullet number two, it says here avoid

bullet number two, it says here avoid dejoxin and stuff like that. Any drug

dejoxin and stuff like that. Any drug that increases the inotropic effect of

that increases the inotropic effect of the heart theoretically can worsen it.

the heart theoretically can worsen it. So negative inotropes

So negative inotropes are the treatment. So it almost again is

are the treatment. So it almost again is a little bit counterintuitive because

a little bit counterintuitive because you know negative inotropes

you know negative inotropes sort of sound like why would I want to

sort of sound like why would I want to give that to a condition of you know

give that to a condition of you know cardiammyopathy

cardiammyopathy uh or in heart failure. Well remember

uh or in heart failure. Well remember it's remodeling benefit so you're you're

it's remodeling benefit so you're you're you're not the negative inotropic

you're not the negative inotropic situation but in in this by slowing down

situation but in in this by slowing down that force of contraction or reducing

that force of contraction or reducing the inotropy allows more less boeing

the inotropy allows more less boeing around that obstruction. I don't know if

around that obstruction. I don't know if that made sense. Um, but you have to

that made sense. Um, but you have to actually see and we probably should have

actually see and we probably should have an image here to show you if if it's not

an image here to show you if if it's not ringing a bell. So, just Google it if

ringing a bell. So, just Google it if you're not sure what hokum is. Uh, but

you're not sure what hokum is. Uh, but it starts to make sense that when it

it starts to make sense that when it that ventricle contracts wrongly. And

that ventricle contracts wrongly. And then ICD n uh ICD placement which is a

then ICD n uh ICD placement which is a defibrillator to prevent them from going

defibrillator to prevent them from going into sudden cardiac death. Anything else

into sudden cardiac death. Anything else there?

there? >> No. Uh I mean I was a distance runner in

>> No. Uh I mean I was a distance runner in college so I actually knew a few people

college so I actually knew a few people that came along with that. So it it is

that came along with that. So it it is not I mean it's it's hard to perceive on

not I mean it's it's hard to perceive on normal screening but in certain

normal screening but in certain situations they can identify it. So yeah

situations they can identify it. So yeah because people look healthy they look

because people look healthy they look normal they're athletes you know and

normal they're athletes you know and then they pass out. So hypertension not

then they pass out. So hypertension not to insult anybody's intelligence here.

to insult anybody's intelligence here. Obviously there's essential hypertension

Obviously there's essential hypertension and there's secondary hypertension. You

and there's secondary hypertension. You always got to make sure you're not

always got to make sure you're not ruling out secondary like the cocaine

ruling out secondary like the cocaine user. uh the patient with aldoststerone

user. uh the patient with aldoststerone hyperldsteroneism,

hyperldsteroneism, you know, that kind of stuff that you

you know, that kind of stuff that you want to, you know, that might be treated

want to, you know, that might be treated differently. So, but your goal is to get

differently. So, but your goal is to get the left to 130 over 80. Um, clearly

the left to 130 over 80. Um, clearly when you think about monotherapy

when you think about monotherapy firstline treatments,

firstline treatments, okay, there may be some ethnicity and,

okay, there may be some ethnicity and, you know, gender uh issues that you

you know, gender uh issues that you might want to consider and certainly

might want to consider and certainly special population. So, if they're

special population. So, if they're pregnant, no aces, no ARBs, just don't

pregnant, no aces, no ARBs, just don't even go there. Okay. uh black patients

even go there. Okay. uh black patients uh again probably aces and arbs as

uh again probably aces and arbs as monotherapy

monotherapy probably not effective. Secondary

probably not effective. Secondary treatments or adjuncts absolutely. So

treatments or adjuncts absolutely. So first line you got your calcium channel

first line you got your calcium channel blockers in particular like amloopines

blockers in particular like amloopines those kind of drugs. Um you got your

those kind of drugs. Um you got your aces your arbs unless they're uh black

aces your arbs unless they're uh black or African-American. Again monotherapy

or African-American. Again monotherapy but most patients are going to need two

but most patients are going to need two and sometimes even three agents um in

and sometimes even three agents um in that situation. So if they are pregnant

that situation. So if they are pregnant uh some people you know like to use or

uh some people you know like to use or consider hydraazine those kind of things

consider hydraazine those kind of things but probably the preferred agent that is

but probably the preferred agent that is more likely to be on the boards is ledol

more likely to be on the boards is ledol maybe a calcium channel blocker in

maybe a calcium channel blocker in particular because uh neither one of

particular because uh neither one of those would also uh put them in preterm

those would also uh put them in preterm labor or anything like that. Anything

labor or anything like that. Anything else here? No. No. I think that's I

else here? No. No. I think that's I think that's good. Again large topic but

think that's good. Again large topic but that that that hits a lot of the key

that that that hits a lot of the key word points there.

word points there. >> Yeah. So Dr. Koko uh very nicely talked

>> Yeah. So Dr. Koko uh very nicely talked about the difference in hypertensive

about the difference in hypertensive crisis and emergencies uh when we have

crisis and emergencies uh when we have patients with target organ damage and

patients with target organ damage and aorta and dissection is clearly one of

aorta and dissection is clearly one of those. So this is everything but that.

those. So this is everything but that. All right. So uh but target organs are

All right. So uh but target organs are the brain. So stroke, going blind, the

the brain. So stroke, going blind, the aorta, heart attack, renal failure.

aorta, heart attack, renal failure. Those are the most common

Those are the most common uh reasons for a hypertensive emergency.

uh reasons for a hypertensive emergency. Uh outside of that, other secondary

Uh outside of that, other secondary causes would be uh patients who are

causes would be uh patients who are preeacclamptic

preeacclamptic um that are impregn um that would be

um that are impregn um that would be kind of another situation that can

kind of another situation that can become especially if they have eclampsia

become especially if they have eclampsia a problem. Um but when you have these

a problem. Um but when you have these patients with a target organ damage

patients with a target organ damage uh affecting you want to bring the blood

uh affecting you want to bring the blood pressure down. So many times their blood

pressure down. So many times their blood pressure systolics over 180 and their

pressure systolics over 180 and their diastolics over 120. And again, if

diastolics over 120. And again, if you're in the context of a es schemic

you're in the context of a es schemic stroke, you got to get that down. Okay?

stroke, you got to get that down. Okay? Um, you got to keep that under control.

Um, you got to keep that under control. Um, and so that's where your uh IV or

Um, and so that's where your uh IV or parental agents are many times going to

parental agents are many times going to be useful, especially if you can titrate

be useful, especially if you can titrate it. And you want again about a 25%

it. And you want again about a 25% reduction in the MAP. Uh, you know, and

reduction in the MAP. Uh, you know, and that's done over a period of, you know,

that's done over a period of, you know, one to four hours. So it's not just like

one to four hours. So it's not just like sudden like drop because especially if

sudden like drop because especially if it's in the brain, right? and you have a

it's in the brain, right? and you have a a lesion and you drop their pressure too

a lesion and you drop their pressure too quickly too fast, you could hypo perfuse

quickly too fast, you could hypo perfuse the tissue distal to the occlusion. So

the tissue distal to the occlusion. So when we talk about rapid pulse and rapid

when we talk about rapid pulse and rapid systolic reductions that are drastic,

systolic reductions that are drastic, it's only in in the context of aortic

it's only in in the context of aortic dissection. So cleopene is basically a

dissection. So cleopene is basically a very short acting IV infusion. It's like

very short acting IV infusion. It's like esmal but it's your I uh dirop

esmal but it's your I uh dirop non-droparian calc no your dioproparian

non-droparian calc no your dioproparian calcium channel blocker um similar to

calcium channel blocker um similar to esmalol you have obviously nicaropene

esmalol you have obviously nicaropene which is more commonly used in clinical

which is more commonly used in clinical practice by most people led and then of

practice by most people led and then of course nitroglycerin magnesium sulfate

course nitroglycerin magnesium sulfate would be for the pregnant patient with

would be for the pregnant patient with eclampsia.

eclampsia. >> Uh

>> Uh what else? Anything else here? Uh I mean

what else? Anything else here? Uh I mean yeah I think I think that that's a good

yeah I think I think that that's a good uh kind of summary the cleopene just

uh kind of summary the cleopene just caveat it's kind of like propall where

caveat it's kind of like propall where it's a white uh liquid but instead of a

it's a white uh liquid but instead of a 10% emulsion which is propal it's a 20%

10% emulsion which is propal it's a 20% emulsion you'd think that increased lip

emulsion you'd think that increased lip is higher it actually doesn't which is

is higher it actually doesn't which is kind of interesting but uh it's very

kind of interesting but uh it's very rapid easy to titrate although nicartine

rapid easy to titrate although nicartine is also in the same boat uh pretty easy

is also in the same boat uh pretty easy to adjust but much longer halflife

to adjust but much longer halflife >> absolutely so good yeah the lipid

>> absolutely so good yeah the lipid emulsion problem like with propalls is

emulsion problem like with propalls is the same potential issue. And then it is

the same potential issue. And then it is very expensive. I' I've never even seen

very expensive. I' I've never even seen it used clinically.

it used clinically. >> Um I know I'm not allowed to order it.

>> Um I know I'm not allowed to order it. >> They won't let me. I'm just kidding.

>> They won't let me. I'm just kidding. >> Yeah.

>> Yeah. >> We don't stock it either. That's fine.

>> We don't stock it either. That's fine. >> Right. Uh special populations. Uh what

>> Right. Uh special populations. Uh what are we what are we trying to go here?

are we what are we trying to go here? Oh, what's the deal with this?

Oh, what's the deal with this? Oh. Oh, I think what this is talking

Oh. Oh, I think what this is talking about is um

about is um patients that have secondary causes of

patients that have secondary causes of hypertension. So, you know, you start

hypertension. So, you know, you start thinking about polycystic ovarian

thinking about polycystic ovarian dysfunction. They have insulin

dysfunction. They have insulin resistance. These these typ typically

resistance. These these typ typically have that the metabolic syndrome

have that the metabolic syndrome pattern. Uh they tend to have a lot of

pattern. Uh they tend to have a lot of more uh renin and aldoststerone

more uh renin and aldoststerone function. And so drugs that have

function. And so drugs that have metocoid antagonist activity actually

metocoid antagonist activity actually have very effective use in peacos

have very effective use in peacos patients. patients with

patients. patients with hyperaldostoneism.

hyperaldostoneism. Um so you'll see the electrolyte

Um so you'll see the electrolyte abnormalities where you have the

abnormalities where you have the hyperetriia hypocalemia distribution

hyperetriia hypocalemia distribution um sort of p you know on their labs and

um sort of p you know on their labs and their screening and they're not

their screening and they're not responding to the traditional agents. Uh

responding to the traditional agents. Uh so that's just a thing that you want to

so that's just a thing that you want to um consider with those. All right.

um consider with those. All right. Paricardial tamponod uh this is

Paricardial tamponod uh this is increased intraaricardial pressure. So

increased intraaricardial pressure. So there the membrane around the heart

there the membrane around the heart there's a layer between that and the the

there's a layer between that and the the heart not very much there's a little bit

heart not very much there's a little bit of fluid in there as the heart is

of fluid in there as the heart is beating to kind of le keep it lubed and

beating to kind of le keep it lubed and moving and loose and fluid accumulates

moving and loose and fluid accumulates in there uh or gets in there for some

in there uh or gets in there for some reason and blood accumulates then and

reason and blood accumulates then and basically it can tampon or put pressure

basically it can tampon or put pressure inwardly and basically the the heart

inwardly and basically the the heart can't ex relax and expand and contract

can't ex relax and expand and contract and so it doesn't even fill up and they

and so it doesn't even fill up and they can go into pea arrest test. So you'll

can go into pea arrest test. So you'll see electrical activity trying to go

see electrical activity trying to go through the heart, but there's no pulse

through the heart, but there's no pulse because you're not able to fill the

because you're not able to fill the ventricle and then it's not contracting

ventricle and then it's not contracting enough to get a stroke volume

enough to get a stroke volume sufficient. Um, and so these basically

sufficient. Um, and so these basically have beex triad. They become hypotensive

have beex triad. They become hypotensive from the reduced cardiac output and then

from the reduced cardiac output and then it backs up because the preload is not

it backs up because the preload is not coming back to the heart. So you get

coming back to the heart. So you get JVD, you get these muffled heart sounds

JVD, you get these muffled heart sounds because the fluid is accumulating. you

because the fluid is accumulating. you can't really hear it very well. Um, and

can't really hear it very well. Um, and this is a medical emergency. Uh, when

this is a medical emergency. Uh, when this happens, especially if they go into

this happens, especially if they go into pea arrest. So, the if it's if it's PA,

pea arrest. So, the if it's if it's PA, obviously not for your boards, you stick

obviously not for your boards, you stick a needle in it, drain it. So, literally

a needle in it, drain it. So, literally I stick a needle subzyphoid under

I stick a needle subzyphoid under ultrasound, aspirate the blood out or

ultrasound, aspirate the blood out or the fluid. Like if they have lupus, uh,

the fluid. Like if they have lupus, uh, we see that sometimes in them they'll

we see that sometimes in them they'll develop these pericardial eusions. um

develop these pericardial eusions. um and they can be symptomatic in that

and they can be symptomatic in that situation. Um so you you you you drain

situation. Um so you you you you drain it and you can leave a drain in. They

it and you can leave a drain in. They have to go to surgery. Surgery will cut

have to go to surgery. Surgery will cut a little window out. So it just

a little window out. So it just basically leaks out into the paritinium

basically leaks out into the paritinium itself. So it's a non it you give

itself. So it's a non it you give fluids. I'm sorry. The probably the

fluids. I'm sorry. The probably the other treatment should be on here is IV

other treatment should be on here is IV fluids to maximize preload. Uh but you

fluids to maximize preload. Uh but you got to get rid of that fluid if they go

got to get rid of that fluid if they go into arrest. Pericarditis. This is the

into arrest. Pericarditis. This is the inflammation of the paricardium

inflammation of the paricardium and there's a number of reasons you can

and there's a number of reasons you can see that drugs can do that. Um so the

see that drugs can do that. Um so the classic medications like hydrazine

classic medications like hydrazine procanomide that have been associated

procanomide that have been associated with that. um you have in infections um

with that. um you have in infections um and uh you know mainly viral and any

and uh you know mainly viral and any virus can do it can cause myocarditis

virus can do it can cause myocarditis and pericarditis and they come in with

and pericarditis and they come in with these chest pains and um so it's it kind

these chest pains and um so it's it kind of confuses things and of course lupus

of confuses things and of course lupus um you get the extra articular and uh

um you get the extra articular and uh involvement you get the vascular

involvement you get the vascular involvement. This is another example of

involvement. This is another example of other tissues that are affected like the

other tissues that are affected like the vasculature and and such. Um, so they

vasculature and and such. Um, so they come in with chest pain and they'll

come in with chest pain and they'll classically say that it improves with

classically say that it improves with leaning forward uh and was worsening

leaning forward uh and was worsening laying back. So if they say, "My chest

laying back. So if they say, "My chest pain worsens when I'm laying back in

pain worsens when I'm laying back in bed." Uh, that's classic. When you do an

bed." Uh, that's classic. When you do an EKG, you see these ST segment elevations

EKG, you see these ST segment elevations and you go, "Oh my gosh, is the patient

and you go, "Oh my gosh, is the patient having a STEMI?" And the answer is no.

having a STEMI?" And the answer is no. because you don't see you see ST segment

because you don't see you see ST segment elevations in all of the leads which if

elevations in all of the leads which if all the vessels in the coronary all the

all the vessels in the coronary all the coronary vessels were accluded they'd be

coronary vessels were accluded they'd be in arrest so so that's not the case uh

in arrest so so that's not the case uh but it's irritating the myioardium

but it's irritating the myioardium and it's causing inflammation which is

and it's causing inflammation which is affecting the uh uh ax potential

affecting the uh uh ax potential movement through the uh myioardium and

movement through the uh myioardium and it's causing that ST segment

it's causing that ST segment elevation that is widespread So because

elevation that is widespread So because you have inflammation whatever the

you have inflammation whatever the culprit so remove the underlying problem

culprit so remove the underlying problem if it's a drug but you still have to

if it's a drug but you still have to treat the inflammation and so post

treat the inflammation and so post myioardial inffection um

myioardial inffection um uh which occurs about two to three weeks

uh which occurs about two to three weeks afterwards um aspirin sometimes people

afterwards um aspirin sometimes people add on cultine um to reduce that but

add on cultine um to reduce that but it's up to three months when you do that

it's up to three months when you do that and then certainly if they have a fusion

and then certainly if they have a fusion so you got to get some of that off. Greg

so you got to get some of that off. Greg anything else here? Yeah, I mean just

anything else here? Yeah, I mean just with the cultureine if it is an option

with the cultureine if it is an option it is a higher dose. It's a twice a day

it is a higher dose. It's a twice a day dose actually compared to what you'd use

dose actually compared to what you'd use it for gout. So there's some dosing

it for gout. So there's some dosing discrepancy with that but um other than

discrepancy with that but um other than that nothing nothing

that nothing nothing >> y here

>> y here >> and one side effect of cultureine

>> and one side effect of cultureine chronically is because of its effects on

chronically is because of its effects on microtubules is bone marrow suppression.

microtubules is bone marrow suppression. >> Yeah absolutely

>> Yeah absolutely >> you just got to keep it in the back of

>> you just got to keep it in the back of your mind. It's one of those moning

your mind. It's one of those moning parameters one of those potential

parameters one of those potential adverse reactions or risks. Um it's also

adverse reactions or risks. Um it's also associated with drug interactions. So it

associated with drug interactions. So it can cause meioitis amalgia if it

can cause meioitis amalgia if it accumulates through I think inhibition

accumulates through I think inhibition of 384. So just keep that in the back of

of 384. So just keep that in the back of your mind. All right. P A this is almost

your mind. All right. P A this is almost like the acute limb eskeeia. Um it's

like the acute limb eskeeia. Um it's kind of like coronary artery disease but

kind of like coronary artery disease but it's just in the periphery. So you know

it's just in the periphery. So you know when you're eating that pizza

I like pizza. When you're eating that text mess,

text mess, that's Mexican food in Texas because

that's Mexican food in Texas because that's where I'm from. Sorry you guys

that's where I'm from. Sorry you guys outside of Texas, but we got the best

outside of Texas, but we got the best Mexican food on the planet.

Mexican food on the planet. Piso, chips,

Piso, chips, >> true.

>> true. >> All of that does not just selectively

>> All of that does not just selectively route itself to the coronary artery. It

route itself to the coronary artery. It will distribute everywhere. Okay? And so

will distribute everywhere. Okay? And so that's where people can again develop

that's where people can again develop you know arterial disease where they

you know arterial disease where they have an ABI that is less than uh 0.9. So

have an ABI that is less than uh 0.9. So if a portion of that athoscrotic plaque

if a portion of that athoscrotic plaque breaks off and it travels down distal

breaks off and it travels down distal then it's eventually going to olude and

then it's eventually going to olude and everything distal that point is now

everything distal that point is now eskeemic. And that's why if somebody

eskeemic. And that's why if somebody comes in with a a finger or a hand or a

comes in with a a finger or a hand or a leg or extremity that is acutely

leg or extremity that is acutely discolored

discolored change in temperature and is

change in temperature and is excruciating pain out of proportion

excruciating pain out of proportion that is a and you can't feel a pulse or

that is a and you can't feel a pulse or get capillary refill that is an arterial

get capillary refill that is an arterial uh emergency just like we talked about

uh emergency just like we talked about earlier uh before. So you want to treat

earlier uh before. So you want to treat the underlying problem no different than

the underlying problem no different than a coronary artery disease. So treat

a coronary artery disease. So treat their blood pressure, treat their

their blood pressure, treat their dysipidemia. If they have

dysipidemia. If they have hyperhomocymia, if they have

hyperhomocymia, if they have uncontrolled diabetes, get all that

uncontrolled diabetes, get all that stuff under control. Uh drugs that uh

stuff under control. Uh drugs that uh will reduce obviously platelet

will reduce obviously platelet aggregation and emblei formation,

aggregation and emblei formation, aspirin because this is an arterial

aspirin because this is an arterial problem, not a venus problem. So it's

problem, not a venus problem. So it's not anti-coagulants.

not anti-coagulants. Only where antiquagulants come in is in

Only where antiquagulants come in is in severe disease or an acute eskeemic

severe disease or an acute eskeemic event.

event. um ACE inhibitors uh because of their

um ACE inhibitors uh because of their effects on the remodeling of the

effects on the remodeling of the vasculature

vasculature can help maintain that blood flow and

can help maintain that blood flow and prevent remodeling and then you know

prevent remodeling and then you know plus or minus maybe some ptoxifilene

plus or minus maybe some ptoxifilene which may help those you know the

which may help those you know the the red blood cell and stuff like that

the red blood cell and stuff like that kind of move through there a little

kind of move through there a little easier. Um all right pulmonary

easier. Um all right pulmonary hypertension there

hypertension there are a number of different so world

are a number of different so world health organization has a number of

health organization has a number of classes and it's based on the underlying

classes and it's based on the underlying problem. So but what ultimately happens

problem. So but what ultimately happens is the portal the pulmonary artery

is the portal the pulmonary artery portal pressure the pulmonary artery

portal pressure the pulmonary artery pressures which are typically a low

pressures which are typically a low pressure systems experience high

pressure systems experience high pressure for some reason. So let's just

pressure for some reason. So let's just say it's a PE. Well, if you put a PE, it

say it's a PE. Well, if you put a PE, it comes from your leg. It goes up into the

comes from your leg. It goes up into the uh uh inferior vennea into the right

uh uh inferior vennea into the right atrium, down through the right

atrium, down through the right ventricle, and out the pulmonary artery.

ventricle, and out the pulmonary artery. And let's say it's not massive enough to

And let's say it's not massive enough to cause cardiac arrest or hypotension,

cause cardiac arrest or hypotension, but it's putting pressure, it's

but it's putting pressure, it's preventing flow past that point. So the

preventing flow past that point. So the now the low pressure system is having to

now the low pressure system is having to squeeze harder to overcome that. Well,

squeeze harder to overcome that. Well, then that's the underlying problem. If

then that's the underlying problem. If you have problems with the endovvascular

you have problems with the endovvascular lining not making vaso diilators

lining not making vaso diilators like prostate and local or indogenous

like prostate and local or indogenous nitro nitric oxide then then you're not

nitro nitric oxide then then you're not getting the dilation okay that's keeping

getting the dilation okay that's keeping those pressures there and so you

those pressures there and so you basically see rightsided heart failure

basically see rightsided heart failure occurring so core pulmonal or right side

occurring so core pulmonal or right side of heart failure see JVD okay they

of heart failure see JVD okay they usually don't have lung problems s

usually don't have lung problems s because it's backing up before the

because it's backing up before the lungs. So, JBD, he hpatogular reflex,

lungs. So, JBD, he hpatogular reflex, lower extremity, pitting edema. Uh, the

lower extremity, pitting edema. Uh, the way you diagnose this is an echo. So,

way you diagnose this is an echo. So, you can look at the size of the

you can look at the size of the pulmonary artery. You can measure

pulmonary artery. You can measure pressures and wedge pressures. You can

pressures and wedge pressures. You can do a a cath, a right-sided heart

do a a cath, a right-sided heart catheterization and measure those

catheterization and measure those pressures in there. Um, and so multiple

pressures in there. Um, and so multiple workup things are done to help you

workup things are done to help you assess that. So what you see on this

assess that. So what you see on this slide is based on the underlying problem

slide is based on the underlying problem kind of drives you to the preferred

kind of drives you to the preferred treatment. So World Health Organization

treatment. So World Health Organization groups one and four may have a PE or

groups one and four may have a PE or antiquag a plaque or I mean sorry athos

antiquag a plaque or I mean sorry athos clot formation as being part of the

clot formation as being part of the problem. So that makes sense. Okay. uh

problem. So that makes sense. Okay. uh if you need something to dilate your

if you need something to dilate your calcium channel blockers like nifetapene

calcium channel blockers like nifetapene um amloopene can be helpful your groups

um amloopene can be helpful your groups two and three now you're starting to use

two and three now you're starting to use your endothelon one receptor antagonists

your endothelon one receptor antagonists and your type five phosphodess

and your type five phosphodess inhibitors in different doses than you

inhibitors in different doses than you would use for erectile uh dysfunction so

would use for erectile uh dysfunction so you know erectile dysfunction drugs like

you know erectile dysfunction drugs like selenaphil and varagra were originally

selenaphil and varagra were originally being studied in pulmonary hypertension

being studied in pulmonary hypertension During the clinical trials when all the

During the clinical trials when all the old men started hitting on the nurses,

old men started hitting on the nurses, the research coordinators were like,

the research coordinators were like, "What in the world's going on?" And

"What in the world's going on?" And Fizer finally figured out, "Uhoh,

Fizer finally figured out, "Uhoh, we got a gold blank. Who cares about

we got a gold blank. Who cares about pulmonary hypertension? Let's go for the

pulmonary hypertension? Let's go for the ED." So they went for the ED first,

ED." So they went for the ED first, maxed out that and then came back and

maxed out that and then came back and brought back the pulmonary hypertension

brought back the pulmonary hypertension indication later after they milked it.

indication later after they milked it. But the dosing is different. Craig,

But the dosing is different. Craig, anything here?

anything here? >> Uh no. Uh I mean I I would echo there. I

>> Uh no. Uh I mean I I would echo there. I mean from the first time I learned about

mean from the first time I learned about pulmonary hypertension, there's two

pulmonary hypertension, there's two classifications. Yeah. Now it's up to

classifications. Yeah. Now it's up to six uh based on the different subtypes

six uh based on the different subtypes and the physiology that's been

and the physiology that's been developed. So it's it's it's definitely

developed. So it's it's it's definitely an emerging still ongoing uh process but

an emerging still ongoing uh process but as you mentioned the different groups

as you mentioned the different groups from who have different drug therapies

from who have different drug therapies just emphasize the key drug therapies in

just emphasize the key drug therapies in that and I think that would uh kind of

that and I think that would uh kind of be valuable in this section for sure.

be valuable in this section for sure. Yeah. And if you guys struggle with any

Yeah. And if you guys struggle with any of these concepts or want to go a little

of these concepts or want to go a little bit deeper now remember we have

bit deeper now remember we have individual topics on these

individual topics on these >> in more detail in your account. So if

>> in more detail in your account. So if you need to go back, I mean part of this

you need to go back, I mean part of this is helping you to hopefully brush off

is helping you to hopefully brush off the cobwebs and remember some of that,

the cobwebs and remember some of that, but if you have to go back and look at

but if you have to go back and look at it again, these are those kind of

it again, these are those kind of splitting hair questions. So cardiogenic

splitting hair questions. So cardiogenic shock. So this relates to usually a

shock. So this relates to usually a heart attack in most cases, some sort of

heart attack in most cases, some sort of event uh like a STEMI u has occurred and

event uh like a STEMI u has occurred and so you put them in acute basically heart

so you put them in acute basically heart failure. Okay. So their systolic blood

failure. Okay. So their systolic blood pressure is less than 90. They're

pressure is less than 90. They're usually wet in the lungs. they're having

usually wet in the lungs. they're having hypo profusion of the organs. What

hypo profusion of the organs. What organs? Well, it can be your brain. So,

organs? Well, it can be your brain. So, you're not, you know, have you don't

you're not, you know, have you don't feel, you know, like you're getting good

feel, you know, like you're getting good flow. Your kidneys go into acute kidney

flow. Your kidneys go into acute kidney injury because you're getting hypo

injury because you're getting hypo profusion into the renal apherin

profusion into the renal apherin arterial, right? So, those are the

arterial, right? So, those are the typical things that you see. Um, and so

typical things that you see. Um, and so if they are having an event and they're

if they are having an event and they're they're unstable, you might need to

they're unstable, you might need to stabilize them and put them on a number

stabilize them and put them on a number of drips, start a central line and put

of drips, start a central line and put them on basor therapy. And many times,

them on basor therapy. And many times, again, this is a double-edged sword. You

again, this is a double-edged sword. You got a diseased heart where you're

got a diseased heart where you're stimulating the them with agents that

stimulating the them with agents that are actually somewhat proythmic and

are actually somewhat proythmic and increasing oxygen demands, but you got

increasing oxygen demands, but you got an insult. So sometimes it can

an insult. So sometimes it can precipitate the worsening of the

precipitate the worsening of the condition but you got to do something.

condition but you got to do something. All right. So obviously until you can

All right. So obviously until you can treat the underlying cause like go to

treat the underlying cause like go to the cath lab and open them back up and

the cath lab and open them back up and salvage whatever you can and hope they

salvage whatever you can and hope they go by or put them on you know some

go by or put them on you know some people have to go on ECMO or until they

people have to go on ECMO or until they can get an elvad you know placed or

can get an elvad you know placed or something like that to you know help

something like that to you know help correct their situation.

correct their situation. Um so dobbutamine

Um so dobbutamine um higher dose dopamine

um higher dose dopamine uh can certainly increase the inotropic

uh can certainly increase the inotropic effect is certainly Miller known if you

effect is certainly Miller known if you have underlying beta blockers on board

have underlying beta blockers on board and then you have to add on vasopressors

and then you have to add on vasopressors many times especially with doputamine.

many times especially with doputamine. >> So just remember doputamine being a beta

>> So just remember doputamine being a beta 2 receptor agonist as well as beta 1 can

2 receptor agonist as well as beta 1 can cause dilation of the arterial system.

cause dilation of the arterial system. So you might get yes increase in the

So you might get yes increase in the pulse but you're also going to increase

pulse but you're also going to increase in the inotropy which will increase

in the inotropy which will increase stroke volume and cardic output but you

stroke volume and cardic output but you can also dilate them. So you just got to

can also dilate them. So you just got to be real careful when you initiate the

be real careful when you initiate the dopamine be ready in the background to

dopamine be ready in the background to initiate that norepinephrine quickly if

initiate that norepinephrine quickly if they have that response.

they have that response. >> You don't know who who it's always going

>> You don't know who who it's always going to be. Correct. Anything to add on that

to be. Correct. Anything to add on that one?

one? >> No I would I would definitely emphasize

>> No I would I would definitely emphasize that uh clinically. I've experienced

that uh clinically. I've experienced that myself too.

that myself too. >> Okay. All right. hypoalmic shock. So

>> Okay. All right. hypoalmic shock. So obviously some volume. So preload has

obviously some volume. So preload has been dropped that infects the afterload.

been dropped that infects the afterload. Um so you got to figure out why. So if

Um so you got to figure out why. So if it's trauma, well then you need to give

it's trauma, well then you need to give them blood and then sol surgically solve

them blood and then sol surgically solve the problem. Okay? Figure out where

the problem. Okay? Figure out where they're bleeding and stop that bleeding

they're bleeding and stop that bleeding but give them blood. Um if it's for some

but give them blood. Um if it's for some other reason, right? So you know they

other reason, right? So you know they maybe they are just volume depleted

maybe they are just volume depleted they're dehydrated

they're dehydrated whatever you know give them something

whatever you know give them something back because remember one of the five

back because remember one of the five hes and 5ts in pea arrest

hes and 5ts in pea arrest is hypoalmia

is hypoalmia so the heart is fine right but there's

so the heart is fine right but there's no volume so you can't generate a pulse

no volume so you can't generate a pulse and you can't peruse the brain so stop

and you can't peruse the brain so stop and think why is this patient why would

and think why is this patient why would hypoalmic shock be the problem and most

hypoalmic shock be the problem and most commonly associated with some traumatic

commonly associated with some traumatic injury or they have anti-coagulation on

injury or they have anti-coagulation on board and they're bleeding out like a GI

board and they're bleeding out like a GI bleed. Okay, so there's no trauma, but

bleed. Okay, so there's no trauma, but they're bleeding somewhere. Um, and so

they're bleeding somewhere. Um, and so that's why GI bleeds get very

that's why GI bleeds get very problematic and why you need to give

problematic and why you need to give them blood in that situation, especially

them blood in that situation, especially if they're symptomatic. Okay. Um, all

if they're symptomatic. Okay. Um, all right. Neurogenic shock. So this is

right. Neurogenic shock. So this is where they've lost their sort of

where they've lost their sort of sympathetic tone coming from the central

sympathetic tone coming from the central nervous system and they have unopposed

nervous system and they have unopposed parasympathetic intervation and so they

parasympathetic intervation and so they basically get this widespread end organ

basically get this widespread end organ hypo perfusion. So where this somewhat

hypo perfusion. So where this somewhat shows up is in spinal cord injuries. And

shows up is in spinal cord injuries. And the reason that you want to be careful

the reason that you want to be careful of this scenario is when you hypoeruse

of this scenario is when you hypoeruse other organs you're also hyperprofusing

other organs you're also hyperprofusing the brain. And if that spinal cord is

the brain. And if that spinal cord is injured, you want to keep blood flow to

injured, you want to keep blood flow to it as much as possible to hopefully

it as much as possible to hopefully regain some of that function. So, you

regain some of that function. So, you know, as long as it's not severed, you

know, as long as it's not severed, you can regain some some um pressure. So,

can regain some some um pressure. So, you might want to boost the map close to

you might want to boost the map close to the, you know, definitely above 65, but

the, you know, definitely above 65, but closer to 80, some people even say 85 to

closer to 80, some people even say 85 to get that profusion to that um the small

get that profusion to that um the small vessels of the spinal cord.

vessels of the spinal cord. All right, septic shock. So, sepsis is a

All right, septic shock. So, sepsis is a disregulated immunologic response to an

disregulated immunologic response to an infectious process.

infectious process. And when people come in and they're

And when people come in and they're experiencing sepsis, it is that immune

experiencing sepsis, it is that immune response that is out of is that's that's

response that is out of is that's that's problematic. And so, you need to know

problematic. And so, you need to know the surge criteria. They most commonly

the surge criteria. They most commonly have two or more of these. You need to

have two or more of these. You need to remember the extremes. It's not just

remember the extremes. It's not just fever, but it could be hypothermia as

fever, but it could be hypothermia as well. It's not just elevated white blood

well. It's not just elevated white blood cells, but it could be low blood white

cells, but it could be low blood white blood cells. Um, so just keep those

blood cells. Um, so just keep those things in mind as well as a lactic acid

things in mind as well as a lactic acid uh usually over two, especially if

uh usually over two, especially if they're in shock. Okay, SERS is the

they're in shock. Okay, SERS is the criteria up here. And then the QOPA,

criteria up here. And then the QOPA, sorry, QOPA is a score that is more

sorry, QOPA is a score that is more indicative of their prognosis and more

indicative of their prognosis and more done in the ICU setting.

done in the ICU setting. um because you need a bunch of data to

um because you need a bunch of data to plug into that. Uh they're never going

plug into that. Uh they're never going to ask you to memorize it. You you would

to ask you to memorize it. You you would they would give you a sofa score and ask

they would give you a sofa score and ask you to interpret or tell you that's

you to interpret or tell you that's based on sofa score the patient is

based on sofa score the patient is concerned for this. So traditional

concerned for this. So traditional treatment of sepsis is fill the tank as

treatment of sepsis is fill the tank as long as they can handle the fluids. So

long as they can handle the fluids. So around 30 cc per kilo of fluids. um you

around 30 cc per kilo of fluids. um you start empiric antibiotics after the uh

start empiric antibiotics after the uh blood cultures and urine cultures have

blood cultures and urine cultures have been obtained. Um and you want to try to

been obtained. Um and you want to try to do that within the hour if you can. You

do that within the hour if you can. You want to shoot for a goal of mean

want to shoot for a goal of mean arterial pressure of 65 or greater. And

arterial pressure of 65 or greater. And if it's less than that then and you've

if it's less than that then and you've given fluid and you're given those

given fluid and you're given those things and you start uh basor therapy.

things and you start uh basor therapy. Um if that doesn't work you can consider

Um if that doesn't work you can consider either a second basopressor therapy like

either a second basopressor therapy like vasop prein or you could go to

vasop prein or you could go to hydrocortisone which has got mineralic

hydrocortisone which has got mineralic corticore activity. Craig anything else?

corticore activity. Craig anything else? >> Uh yeah I mean that's a good summary. I

>> Uh yeah I mean that's a good summary. I think uh crystalalloid is is certainly a

think uh crystalalloid is is certainly a key here. Can you can hypothetically use

key here. Can you can hypothetically use colloid also but crystalloids NS or LR

colloid also but crystalloids NS or LR um again we've debated that in the past

um again we've debated that in the past too either or in this situation on a on

too either or in this situation on a on a clinical exam I I don't think it makes

a clinical exam I I don't think it makes a difference the norepinephrine as well

a difference the norepinephrine as well just starting that early getting on um

just starting that early getting on um and again in order of uh antibiotic

and again in order of uh antibiotic administration typically it's the

administration typically it's the betalactam first um trying to target the

betalactam first um trying to target the gram negatives and then uh your venkcomy

gram negatives and then uh your venkcomy if they meet criteria and then your

if they meet criteria and then your atypical uh so is

atypical uh so is chloromy or doxycycline if it's a

chloromy or doxycycline if it's a pneumonia consideration on the

pneumonia consideration on the differential. So um the order might be

differential. So um the order might be relevant in that

relevant in that >> absolutely always give the drug that's

>> absolutely always give the drug that's going to great provide the greatest bang

going to great provide the greatest bang for buck first and it's also the fastest

for buck first and it's also the fastest to administer and that's your sephy like

to administer and that's your sephy like that. The other thing to keep in mind is

that. The other thing to keep in mind is when you think of a peric antibiotic

when you think of a peric antibiotic therapy whether it's menitis, sepsis,

therapy whether it's menitis, sepsis, SBP, I don't care what it is, every

SBP, I don't care what it is, every empiric regimen almost always have

empiric regimen almost always have bacterial properties. You are not using

bacterial properties. You are not using bacterial static drugs as the only

bacterial static drugs as the only treatment in these situations. So if you

treatment in these situations. So if you if you get stuck and you even and you

if you get stuck and you even and you know those every one of the empiric

know those every one of the empiric regimens always have a bacterial agent

regimens always have a bacterial agent in there doesn't rely on the immune

in there doesn't rely on the immune system to help you. All right. Syncopy.

system to help you. All right. Syncopy. So there's some loss of blood flow

So there's some loss of blood flow basically to the brain um or some

basically to the brain um or some problem with the brain. It's not getting

problem with the brain. It's not getting enough oxygen. It's not getting enough

enough oxygen. It's not getting enough glucose. Most commonly it's not getting

glucose. Most commonly it's not getting enough blood flow. So you have to treat

enough blood flow. So you have to treat the underlying cause and try to

the underlying cause and try to obviously figure out what's going on.

obviously figure out what's going on. Aortic regge. So this is sort of the

Aortic regge. So this is sort of the opposite of aortic stenosis where the

opposite of aortic stenosis where the the valve in stenosis is stenotic. It's

the valve in stenosis is stenotic. It's real rigid, hard, calcified. Aortic

real rigid, hard, calcified. Aortic regurg the the the valves are loose and

regurg the the the valves are loose and so the doors don't shut. Uh as the blood

so the doors don't shut. Uh as the blood kind of comes back, it just keeps

kind of comes back, it just keeps opening. So blood goes up and it comes

opening. So blood goes up and it comes right back down. Um and so these

right back down. Um and so these patients can develop rapid pulmonary

patients can develop rapid pulmonary edema because it backs up into the left

edema because it backs up into the left ventricle and it backs up into the

ventricle and it backs up into the lungs. Um and so in these patients u

lungs. Um and so in these patients u they need something to fix aorta. This

they need something to fix aorta. This can be an acute life-threatening

can be an acute life-threatening situation. So you want to do whatever

situation. So you want to do whatever you can to reduce um uh the afterload

you can to reduce um uh the afterload and you want to improve inotropy.

and you want to improve inotropy. Okay. chronically uh ACE inhibitors,

Okay. chronically uh ACE inhibitors, calcium channel blockers uh because of

calcium channel blockers uh because of the vascular remodeling. Kawasaki's

the vascular remodeling. Kawasaki's disease also known as muc

disease also known as muc mucoutcutaneous

mucoutcutaneous lymph node syndrome uh these patients

lymph node syndrome uh these patients have and syndrome is a key word that

have and syndrome is a key word that means multiple manifestations or organs

means multiple manifestations or organs being involved. Okay. So it's a a febal

being involved. Okay. So it's a a febal illness that's a vasculitis of the small

illness that's a vasculitis of the small and medium arteries most commonly

and medium arteries most commonly affecting pediatric patients. And so

affecting pediatric patients. And so vasculitis is an inflammation of the

vasculitis is an inflammation of the blood vessels uh and again typically the

blood vessels uh and again typically the arteries and the precipitant many times

arteries and the precipitant many times is unknown but has been linked to viral

is unknown but has been linked to viral illnesses. And so if they have a fever

illnesses. And so if they have a fever for five days and they have to have five

for five days and they have to have five four of the five clinical symptoms. So

four of the five clinical symptoms. So they have a rash on their body. Cervical

they have a rash on their body. Cervical lympadinopathy in the anterior chain or

lympadinopathy in the anterior chain or posterior chain of their necks.

posterior chain of their necks. Bilateral conjunctival injection. So

Bilateral conjunctival injection. So that means they have looks like they

that means they have looks like they have conjunctivitis.

have conjunctivitis. They have oral mucosal changes. They

They have oral mucosal changes. They sometimes their tongue look like

sometimes their tongue look like strawberry. They have real red and

strawberry. They have real red and peeling lips. And then they can have

peeling lips. And then they can have peripheral extremity changes where their

peripheral extremity changes where their skin is peeling on the extremities. Um

skin is peeling on the extremities. Um and that's very classic. you'll see

and that's very classic. you'll see increases inflammatory markers because

increases inflammatory markers because of the vasculitis ESR CRP. Echo

of the vasculitis ESR CRP. Echo cardiogram is done to look for the

cardiogram is done to look for the coronary um aneurysms that can sometimes

coronary um aneurysms that can sometimes form because that drives your therapy.

form because that drives your therapy. Uh these patients if they have coronary

Uh these patients if they have coronary involvement need to be on highdose um

involvement need to be on highdose um aspirin and they also need to be on IVIG

aspirin and they also need to be on IVIG therapy to kind of hit the uh inflam

therapy to kind of hit the uh inflam inflammatory markers. Sometimes uh

inflammatory markers. Sometimes uh steroids or other imunosuppressive

steroids or other imunosuppressive agents are added on but the highdosese

agents are added on but the highdosese aspirin seems counterintuitive.

aspirin seems counterintuitive. >> This is the trick because this is a

>> This is the trick because this is a pediatric patient with a fever

pediatric patient with a fever and viral illness could be the

and viral illness could be the precipitant

precipitant and why don't you want to give aspirin

and why don't you want to give aspirin to a pediatric patient.

to a pediatric patient. theoretically you're worried about ry

theoretically you're worried about ry syndrome, right? So that they don't they

syndrome, right? So that they don't they can go into this delayed hippatic

can go into this delayed hippatic failure

failure which they basically start having

which they basically start having profuse vomiting that's uncontrolled and

profuse vomiting that's uncontrolled and develop in sephylopathy and then die

develop in sephylopathy and then die from dehydration electrolyte

from dehydration electrolyte abnormalities.

abnormalities. So it is a problem but the benefits of

So it is a problem but the benefits of aspirin use in this situation outweigh

aspirin use in this situation outweigh the risk. Anything else here? No, I

the risk. Anything else here? No, I think that was a good key uh

think that was a good key uh differentiation using aspirin highdose

differentiation using aspirin highdose aspirin in a pediatric population that

aspirin in a pediatric population that certainly yeah high dose high

certainly yeah high dose high >> long term very different. Okay, those

>> long term very different. Okay, those are some of the nuances from the boards

are some of the nuances from the boards that they like.

that they like. All right, rayods. Uh so this is a

All right, rayods. Uh so this is a connective tissue disorder um and

connective tissue disorder um and affects predominantly small vessels of

affects predominantly small vessels of the fingers and the toes. And you'll

the fingers and the toes. And you'll probably see pictures of the hands with

probably see pictures of the hands with the fingertips that are all kind of

the fingertips that are all kind of blue, you know, and they look like they

blue, you know, and they look like they change and and it hurt sometimes because

change and and it hurt sometimes because there's lack of blood flow. So they have

there's lack of blood flow. So they have the abnormal cold challenge test. So you

the abnormal cold challenge test. So you want to warm their hands to try to

want to warm their hands to try to basilate those vessels. If that doesn't

basilate those vessels. If that doesn't work, then topical nitroglycerin in

work, then topical nitroglycerin in those areas can help relax some of the

those areas can help relax some of the spasms and help dilate that. If that

spasms and help dilate that. If that doesn't work, then amloopene um and and

doesn't work, then amloopene um and and nenopene which are your digit and

nenopene which are your digit and calcium channel blockers will help relax

calcium channel blockers will help relax those. So you'll see patients commonly

those. So you'll see patients commonly on those or those are acutely used in

on those or those are acutely used in that situation and then avoiding

that situation and then avoiding obviously the triggers which can be many

obviously the triggers which can be many things for that patient, stress,

things for that patient, stress, temperature changes, things like that.

temperature changes, things like that. Okay.

Okay. Temporal arteritis is uh similar to uh

Temporal arteritis is uh similar to uh Kawasakis. It is a vasculitis

Kawasakis. It is a vasculitis involving the uh larger vessels of the

involving the uh larger vessels of the arteries but it particularly this one

arteries but it particularly this one affects the superficial temporal artery

affects the superficial temporal artery which is around this area that has a

which is around this area that has a branch that then goes to the opthalmic

branch that then goes to the opthalmic arteries of your eye. Um and so these

arteries of your eye. Um and so these patients commonly will present with a

patients commonly will present with a clot jaw claudication because your

clot jaw claudication because your jawbone is up here and they have

jawbone is up here and they have headache that's unilateral and

headache that's unilateral and associated with some sort of changes in

associated with some sort of changes in vision. Okay, that's the triad. That is

vision. Okay, that's the triad. That is the concern and when that happens you

the concern and when that happens you need to be very concerned for this

need to be very concerned for this because the risk is they can go blind.

because the risk is they can go blind. So the inflammation of the vessel gets

So the inflammation of the vessel gets so much that it oludes the vessel

so much that it oludes the vessel which reduces distal blood profusion

which reduces distal blood profusion to the eye. Okay. And so you sometimes

to the eye. Okay. And so you sometimes can order ESR CRPS see that they're

can order ESR CRPS see that they're elevated because of the inflammation. Uh

elevated because of the inflammation. Uh opthalmologists will do a uh temporal

opthalmologists will do a uh temporal artery biopsy to prove the diagnosis

artery biopsy to prove the diagnosis because the treatment is also long-term

because the treatment is also long-term treatment for sometimes two years. uh

treatment for sometimes two years. uh predinazone at high doses. And so when

predinazone at high doses. And so when you use doses at this height, you will

you use doses at this height, you will definitely cause HPA suppression plus

definitely cause HPA suppression plus all the other crap.

all the other crap. Um any other things on this one?

Um any other things on this one? >> Uh no, that's a good summary.

>> Uh no, that's a good summary. >> Yeah, just keep in mind though, when you

>> Yeah, just keep in mind though, when you get to that dose, you're exceeding the

get to that dose, you're exceeding the endogenous production of cortisol. You

endogenous production of cortisol. You will get HPA suppression. And if someone

will get HPA suppression. And if someone like this is on doses that high for that

like this is on doses that high for that long, if they find themselves in a

long, if they find themselves in a stressful situation, they will need

stressful situation, they will need basically stress hormone prophylaxis.

basically stress hormone prophylaxis. You're going to have to dose them in the

You're going to have to dose them in the acute situation of surgery or illness or

acute situation of surgery or illness or trauma with higher dose hydrocortisone

trauma with higher dose hydrocortisone therapy or they can get um adrenal

therapy or they can get um adrenal crisis.

crisis. uh DVTs.

uh DVTs. Uh so you have stasis of blood flow

Uh so you have stasis of blood flow through the vascule where blood slows

through the vascule where blood slows down and it starts to interact

down and it starts to interact uh and that forms a clot and that can

uh and that forms a clot and that can that clot can form a thrombus that if it

that clot can form a thrombus that if it stays in the vessel is fine somewhat

stays in the vessel is fine somewhat obviously cause edema and pain but if it

obviously cause edema and pain but if it starts to move then it has imilized and

starts to move then it has imilized and now moves to the lungs and can cause the

now moves to the lungs and can cause the pulmonary emblei. So these patients

pulmonary emblei. So these patients usually present with unilateral leg pain

usually present with unilateral leg pain and swelling some redness. So it gets

and swelling some redness. So it gets confusing if there's a cellulitis over a

confusing if there's a cellulitis over a vasculitis but they develop thrombbo

vasculitis but they develop thrombbo thromboflabitis

thromboflabitis basically inflammation irritation of the

basically inflammation irritation of the of the vein. Um and so in these patients

of the vein. Um and so in these patients uh ultrasound is done to look for uh the

uh ultrasound is done to look for uh the clot ends up finding the clot is there.

clot ends up finding the clot is there. So you have a number of different

So you have a number of different treatment options. Anti-coagulation if

treatment options. Anti-coagulation if they're stable and don't need to be

they're stable and don't need to be admitted. You got a pixaban deigatran

admitted. You got a pixaban deigatran riveroxaban or an oxiparin at full

riveroxaban or an oxiparin at full anti-coagulation doses for at least

anti-coagulation doses for at least three months if it's definitely if it's

three months if it's definitely if it's an unprovoked

an unprovoked uh alternatives are warrin and adoxaban.

uh alternatives are warrin and adoxaban. Um if you develop a PE uh again this has

Um if you develop a PE uh again this has gone to the heart move through the

gone to the heart move through the atrium down the right ventricle out in

atrium down the right ventricle out in the pulmonary artery can cause chest

the pulmonary artery can cause chest pain shortness of breath. If it's bad

pain shortness of breath. If it's bad enough or large enough then it can start

enough or large enough then it can start to cause hemodynamic instability

to cause hemodynamic instability and that can lead to hypotension.

and that can lead to hypotension. The rules that you can use are the perk

The rules that you can use are the perk rule for low-risk patients. If you can't

rule for low-risk patients. If you can't discern who's a lowrisisk patient, do

discern who's a lowrisisk patient, do the well score. Well, score first tells

the well score. Well, score first tells you if it's low, medium, or high risk.

you if it's low, medium, or high risk. If your clinical suspicion is already

If your clinical suspicion is already high, you're going to do a CT angio

high, you're going to do a CT angio anyway. Uh, perk roll is really being

anyway. Uh, perk roll is really being used in a low-risisk patient to help you

used in a low-risisk patient to help you decide if you can rule out PE with no CT

decide if you can rule out PE with no CT scan. So, if they have acute PE, if

scan. So, if they have acute PE, if they're hemodynamically stable, it's

they're hemodynamically stable, it's anti-coagulation. Okay? So if if you you

anti-coagulation. Okay? So if if you you can use unfraction apron if you want to

can use unfraction apron if you want to or noxparent

or noxparent and you can even use oral agents. Okay.

and you can even use oral agents. Okay. Um most people probably admit because

Um most people probably admit because they want to make sure uh and just

they want to make sure uh and just monitor them from 24 hours. But if

monitor them from 24 hours. But if theoretically if they're hemodynamically

theoretically if they're hemodynamically unstable and it's small or a segmental

unstable and it's small or a segmental PE you could get away with potentially

PE you could get away with potentially sending them home if they're very

sending them home if they're very reliable.

reliable. Submassive or massive PE. Now, there's

Submassive or massive PE. Now, there's right-sided manifestations. There's

right-sided manifestations. There's cardiac output problems. There's

cardiac output problems. There's hypotension problems. And these

hypotension problems. And these patients,

patients, um, depending on where you're at, could

um, depending on where you're at, could get intravascular

get intravascular therapies like throbectomy, pull it out,

therapies like throbectomy, pull it out, uh, or you would have to consider tpa.

uh, or you would have to consider tpa. And there's two different dosing

And there's two different dosing regimens for

regimens for still somewhat stable. So, submassive,

still somewhat stable. So, submassive, you can give it over a two-hour

you can give it over a two-hour infusion. If they're in pea arrest, you

infusion. If they're in pea arrest, you don't have two hours.

don't have two hours. The patient's like gone. Okay? So, you

The patient's like gone. Okay? So, you give them a bolus and you follow the

give them a bolus and you follow the next one I think over 15 minutes. I

next one I think over 15 minutes. I always double check it, but

always double check it, but >> you're giving it a whole different way

>> you're giving it a whole different way in pea versus submassive,

in pea versus submassive, >> right?

>> right? >> Um,

>> Um, >> so we we finished on time because I

>> so we we finished on time because I answered questions throughout. Yes, I'm

answered questions throughout. Yes, I'm gonna defend myself on this. So uh you

gonna defend myself on this. So uh you know we've already covered endocrine um

know we've already covered endocrine um stuff infectious disease in the first

stuff infectious disease in the first session. We've done imunologic

session. We've done imunologic phiccogenetic

phiccogenetic cardiovascular hitting both acute and

cardiovascular hitting both acute and chronic so inpatient outpatient topics

chronic so inpatient outpatient topics in all of these topics. What's coming up

in all of these topics. What's coming up next is oncology

next is oncology and we have some outside experts

and we have some outside experts uh who are clinical oncology uh

uh who are clinical oncology uh pharmacists from the University of

pharmacists from the University of Kentucky. That's Dr. Allison Buts and

Kentucky. That's Dr. Allison Buts and Dr. uh Beth Travers. They are rock stars

Dr. uh Beth Travers. They are rock stars and are going to be joining uh us online

and are going to be joining uh us online and we'll be focused on hematology and

and we'll be focused on hematology and oncology.

oncology. Um and as it relates to oncology, it

Um and as it relates to oncology, it will be more as to the

will be more as to the definitely things that people would

definitely things that people would should know for BOP, but it's not going

should know for BOP, but it's not going to be a review of all the over all the

to be a review of all the over all the cancers and all the various issues. It's

cancers and all the various issues. It's going to service most of the nonbecott

going to service most of the nonbecott people, but it doesn't again it's all

people, but it doesn't again it's all supportive care issues.

supportive care issues. Um I think it's gonna be very good. Um

Um I think it's gonna be very good. Um I'm really excited about it. I think

I'm really excited about it. I think everybody whether you're studying BCOP

everybody whether you're studying BCOP or not and or you're in the other exams

or not and or you're in the other exams where you need to know some oncology

where you need to know some oncology will find it very helpful.

will find it very helpful. >> Yeah, absolutely.

>> Yeah, absolutely. >> And then Dr. Koko is going to lead us on

>> And then Dr. Koko is going to lead us on acute care, critical care, toxicology,

acute care, critical care, toxicology, so neurology

so neurology in the I think the fourth session and

in the I think the fourth session and then we finish up and then at the end we

then we finish up and then at the end we have EBM bioatistics and literature

have EBM bioatistics and literature evaluation that I'll do a kind of a

evaluation that I'll do a kind of a rapid review on for about an hour. Um so

rapid review on for about an hour. Um so it's it's it's busy, but I'm hoping

it's it's it's busy, but I'm hoping you're finding this useful. So now we're

you're finding this useful. So now we're going to go ahead to answer questions.

going to go ahead to answer questions. Um there were several of these questions

Um there were several of these questions that um

that um were se a while back. So I'm going to go

were se a while back. So I'm going to go to the first ones. Uh so the this was

to the first ones. Uh so the this was from Jennifer who asked should you get

from Jennifer who asked should you get an echo to rule out vegetation or clot

an echo to rule out vegetation or clot before doing DC cardioversion

before doing DC cardioversion and I I'm assuming that you're talking

and I I'm assuming that you're talking about in uh well if we're talking about

about in uh well if we're talking about SVT

SVT the answer is no.

the answer is no. Most of the time u if somebody's

Most of the time u if somebody's unstable hemodynamically you just have

unstable hemodynamically you just have to fix that scenario otherwise they

to fix that scenario otherwise they could die. So the

could die. So the where vegetations or clots are would

where vegetations or clots are would show up on a board exam is vegetation

show up on a board exam is vegetation would be there's probably an

would be there's probably an endocarditis or infectious disease issue

endocarditis or infectious disease issue going on and you're they're not going to

going on and you're they're not going to have you go down that path. That's going

have you go down that path. That's going to be very clear-cut endocarditis case,

to be very clear-cut endocarditis case, very clear-cut SVT case or AIB with RVR.

very clear-cut SVT case or AIB with RVR. And in a with RVR,

And in a with RVR, >> you you could cardiovert somebody, but

>> you you could cardiovert somebody, but in most cases, these patients aren't

in most cases, these patients aren't needing cardio conversion most cases.

needing cardio conversion most cases. So, I don't think they're going to go

So, I don't think they're going to go there. Um, and if you were strongly

there. Um, and if you were strongly concerned about it, then yes, you would

concerned about it, then yes, you would get the echo, but that's not going to be

get the echo, but that's not going to be a board exam thing. um wasn't rails um

a board exam thing. um wasn't rails um and emphasis and reduced EF absolutely

and emphasis and reduced EF absolutely so those were patients with um New York

so those were patients with um New York heart functional class three uh heart

heart functional class three uh heart failure predominantly um but again keep

failure predominantly um but again keep in mind that um many times those

in mind that um many times those patients are symptomatic right so class

patients are symptomatic right so class C they have fluid issues they're short

C they have fluid issues they're short of breath you know they've got

of breath you know they've got remodeling issues but you could have

remodeling issues but you could have somebody who um

somebody who um still has been on got ACE inhibitor

still has been on got ACE inhibitor therapy, beta blocker therapy, you're

therapy, beta blocker therapy, you're going to still push that drug. Now, if

going to still push that drug. Now, if you use it in stage A, where it would be

you use it in stage A, where it would be used stage A preferentially is if you

used stage A preferentially is if you have somebody with secondary

have somebody with secondary hypertension,

hypertension, uh because remember, you're treating the

uh because remember, you're treating the underlying hypertension

underlying hypertension in patients with heart failure. And when

in patients with heart failure. And when you look at the guidelines and you

you look at the guidelines and you actually break it down, they yes

actually break it down, they yes preferentially focus on ACE inhibitors

preferentially focus on ACE inhibitors and ARBs and uh uh and tresesto these

and ARBs and uh uh and tresesto these type of thing but they're also say but

type of thing but they're also say but don't forget stop smoking don't forget

don't forget stop smoking don't forget hyper lipidmia or disipidemia don't

hyper lipidmia or disipidemia don't forget hypertension management. So it's

forget hypertension management. So it's multiffactorial many times these things

multiffactorial many times these things are not happening in isolation like we

are not happening in isolation like we see in clinical trials.

see in clinical trials. Uh Jordan asked uh what is the best

Uh Jordan asked uh what is the best option to prevent a patient

option to prevent a patient decompensating in acute kidney injury or

decompensating in acute kidney injury or failure?

Um decompensating in what way? I guess um

um I don't know if you're talking about

I don't know if you're talking about cardiovascular

cardiovascular or what. Um

or what. Um but usually acute kidney injury is

but usually acute kidney injury is occurring because of something else. So

occurring because of something else. So you treat the underlying problem. You

you treat the underlying problem. You don't so it's a volume problem. Make

don't so it's a volume problem. Make sure you peruse it. If it's a cardiac

sure you peruse it. If it's a cardiac output problem, improve cardiac output.

output problem, improve cardiac output. Um and that's but also you need to know

Um and that's but also you need to know what is the type of acute kidney injury.

what is the type of acute kidney injury. Is it a pre-renal? Is it intrinsic? Or

Is it a pre-renal? Is it intrinsic? Or is it post-renal?

is it post-renal? Um so that's hard to answer that

Um so that's hard to answer that question. Sorry Jordan, if I didn't

question. Sorry Jordan, if I didn't answer that quote. Uh, great. Uh, SGLT2

answer that quote. Uh, great. Uh, SGLT2 inhibitors for heart failure. Yes. Um,

inhibitors for heart failure. Yes. Um, so that's a new and emerging uh therapy

so that's a new and emerging uh therapy that is definitely makes is making its

that is definitely makes is making its way and does make sense for patients

way and does make sense for patients with dual diseases. Um, and so assuming

with dual diseases. Um, and so assuming they can afford it and there's no other

they can afford it and there's no other contrations that is definitely something

contrations that is definitely something to uh uh consider. Okay.

to uh uh consider. Okay. Thanks Jennifer for bringing that up.

Thanks Jennifer for bringing that up. That's actually a good question too

That's actually a good question too because that's sometimes outside again

because that's sometimes outside again the the boards um will give you complete

the the boards um will give you complete information to where you check boxes of

information to where you check boxes of the drugs they should be on and then

the drugs they should be on and then what else is next and there's going to

what else is next and there's going to be something in there that drives it. So

be something in there that drives it. So if they have dual coorbidities which

if they have dual coorbidities which many times they do then you want to ask

many times they do then you want to ask yourself or look for that make sure then

yourself or look for that make sure then you go why would I not give this before

you go why would I not give this before I say yes.

I say yes. Uh Craig any I mean any

Uh Craig any I mean any >> no

>> no >> okay let's just shoot through these

>> okay let's just shoot through these questions here so

questions here so >> so for heart failure do we maximize the

>> so for heart failure do we maximize the dose of each agent like ACE or ARB or

dose of each agent like ACE or ARB or uh a bladed blocker first before adding

uh a bladed blocker first before adding another agent many times yes so remember

another agent many times yes so remember most clinical trials there are target

most clinical trials there are target doses you want to do everything you can

doses you want to do everything you can to try to achieve those because That's

to try to achieve those because That's where the evidence-based effect is.

where the evidence-based effect is. Theoretically, if you want to be

Theoretically, if you want to be evidence-based, you got to choose or try

evidence-based, you got to choose or try to get to those target doses. And you

to get to those target doses. And you and if you can always treat something

and if you can always treat something with fewer drugs, then do it right. I

with fewer drugs, then do it right. I think that's

think that's somewhat straightforward. All right. So,

somewhat straightforward. All right. So, uh, so the recording, uh, Connie, uh, I

uh, so the recording, uh, Connie, uh, I don't know exactly. It should be up

don't know exactly. It should be up within relatively I think it's within 24

within relatively I think it's within 24 hours. Uh, very good review. Thanks,

hours. Uh, very good review. Thanks, Ruth. Appreciate always nice feedback.

Ruth. Appreciate always nice feedback. Um, gotta go to a shift. Okay. You're

Um, gotta go to a shift. Okay. You're welcome. Sorry, I was just reading

welcome. Sorry, I was just reading through this. Just she's telling us

through this. Just she's telling us she's being kind and respectful that

she's being kind and respectful that she's going without hanging up. Um, so

she's going without hanging up. Um, so thanks. Thanks you guys. Uh, so Amanda

thanks. Thanks you guys. Uh, so Amanda asked, uh, can aptifetide replaceabi?

asked, uh, can aptifetide replaceabi? Um, Craig, do you want to comment?

Um, Craig, do you want to comment? >> It definitely has. Uh yeah, sixomads

>> It definitely has. Uh yeah, sixomads almost rarely use epiphibitide or um

almost rarely use epiphibitide or um >> it's toaban.

>> it's toaban. >> Yeah, turopaab bandan. They're they're

>> 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.

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YouTube Transcript:Session 2 - Live Rapid Review for BPS Exams

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Session 2 - Live Rapid Review for BPS Exams