March 25, 2026 • 34 mins
Pressors save lives, but only when they match the real problem. Dr. Matthew Harmon joins us to decode how norepinephrine, phenylephrine, and vasopressin change vascular tone, cardiac output, and organ perfusion—and how to pick the right one under pressure.
We start with a crisp hemodynamic framework: MAP as the product of cardiac output and SVR, and stroke volume shaped by preload, contractility, and afterload. From there, we translate receptor pharmacology into bedside choices so you can raise pressure without stealing flow.
We walk through why norepinephrine’s strong alpha-1 with modest beta-1 support often makes it a go-to for septic shock and low EF patients, delivering perfusion pressure while keeping heart rate and myocardial oxygen demand in check. Phenylephrine earns its place for anesthetic-induced hypotension and aortic stenosis by tightening vessels and slowing the heart, but we call out its hidden tax on flow when contractility lags.
Then we pivot to vasopressin’s V1 pathway, ideal for catecholamine-resistant vasodilation, ACE inhibitor–induced vasoplegia, and acidotic states where adrenergic drugs stumble—plus practical dosing that avoids gut and skin hypoperfusion.
Throughout, we focus on individualizing MAP targets, honoring cerebral and renal autoregulation, and protecting patients in high-risk scenarios like sitting shoulder surgery. You’ll hear why short-acting agents beat long-acting antihypertensives intraop, how to convert ICU drip instincts to precise push-dose habits, and when to rethink nitrous, ephedrine, and ketamine.
We also share CRNA interview prep you can use today: anchor answers in ACLS and PALS, show your receptor-level reasoning, and explain not just what you’d do, but why.
If you’re an ICU nurse eyeing anesthesia, or a practicing provider sharpening your pressor playbook, this session brings clarity you can use on your next case. Subscribe, share with a teammate who loves clean hemodynamics, and leave a review with your favorite pressor pearl.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Jenny Finnell (00:00):
Welcome to the CRM School Park Family Comcast,
where we have helped combinemore than 10,000 IC nurses on
their path towards CRMA school.
Our mission is to combineeducation, guidance, and
professional health so you canmove comfortably towards your
dream of becoming a CRMA.
Whether you're still a nursingschool or a seasoned IC nurse.
This podcast is here for you.
(00:21):
Let's get into today's episode.
Welcome back to Cyrus CoverAcademy Podcast.
Today you're listening to one ofour faculty web sessions, stream
live on CSPA's Instagram.
Depend on the day, this may bean open QA where we take your
questions in real time or afocus company discussion where
we go deep on the area that canstrengthen your knowledge and
build your confidence.
If you want to follow along,join us live, make sure to
(00:42):
follow CSPA on Instagram andwatch for session announcements.
You can also join CSPA's freecommunity where we'll share the
schedule of upcoming sessions.
When you tune in live, you canask questions, get clarity on
the spot, and then learnalongside other nurses
navigating the same path.
And as a quick reminder aboutwho you're learning from, every
session is led by CSPA coachesand faculty who are deeply
committed to your success inpursuing this career.
(01:04):
Without further ado, let's getinto today's show.
Dr. Harmon (01:08):
Hello, everybody.
My name is Dr.
Matthew Harmon.
I'm one of the faculty coacheswith CSPA.
I've got almost nine yearsexperience as a CRNA and have
been in academia for the lastfive and a half, almost six
years.
So today we're going to do avasopressor review.
(01:29):
We're going to go ahead and lookat some principles on
vasopressor usage, some thingsyou need to know whenever you're
thinking about CRNA school.
And then we'll open it up for alittle Q ⁇ A here in just a
little bit.
But before we do, I want toremind everybody, we have our
live conference, uh in-personconference for CSPA in
(01:50):
Louisville, Kentucky in June.
So check check that out and viewour free community via the link
tree in our bio.
So when it comes to choosing theright agent or the right
vasopressor, you need to thinkabout the principles you know as
an ICU nurse.
And then also you need to thinkabout what you may need to know
(02:11):
when it comes time for yourinterview.
So you type rate and you usevasopressors every day.
What we want to see in the cRNAworld is that you understand the
receptor pharmacology, thevascular pathophysiology, and
the hemodynamic responses andexpected responses of each drug.
(02:33):
We're going to talk aboutnorepine, phenolephrine, and
vasopressin, and really how thedifferent alpha and beta
receptors translate into realphysiologic effects.
So think about the hemodynamicframework here.
Think about mean arterialpressure.
It's determined by cardiacoutput and times systemic
vascular resistance.
(02:54):
So MAP is going to equal cardiacoutput times SVR.
When you think about cardiacoutput, that's going to be heart
rate multiplied by strokevolume.
Now, stroke volume is going todepend on your preload, your
contractility, and yourafterload.
When we think about hypotension,especially in anesthesia, and
and truthfully, septic shock aswell, this is going to be caused
(03:16):
by that pathophysiologicvasodilation.
This is from inflammatorymediators, and oftentimes our
anesthetic agents cause thatphysiologic vasodilation.
This can lead to a drop in ourSVR.
And this can be sometimesprofound, depending on if the
patient is hypopholemic,positioning in anesthesia, uh
(03:38):
venous pooling.
So vasopressors, by far andlarge, they work to restore that
vascular tone.
Okay?
When you think of restoringintravascular volume, that's
going to be more akin to uhcrystalloids, uh, maybe some
larger colloids as well.
But for our vasopressor agents,we're thinking vascular tone.
(03:59):
Let's really start looking atthe one that most people are
familiar with that you probablyuse every single day, and that's
gonna be norepinephrine.
Norepinephrine has very strongalpha-1 agonism and some mild
beta-1 agonism.
Oftentimes in anesthesia, wethink of norepinephrine as the
more balanced of our vasopressoragents.
(04:22):
So, alpha-1 receptor activation,this is gonna cause that smooth
muscle contraction.
And this is by thatintracellular calcium, as it
increases in that vascularsmooth muscle, those vascular
smooth muscle cells.
This is gonna lead tovasoconstriction, an increase in
your SVR, and an increase inyour MAP.
(04:43):
Now, that beta-1 stimulation,this increases your uh cyclic
AMP and those caritic myocytes.
This leads to that calciuminflux, and this is going to
enhance or augment thatmyocardial contractility.
In anesthesia, whenever you'recoming off of bypass and you're
wanting to enhance thatmyocardial contractility,
oftentimes we're using calcium.
(05:06):
So whenever you contrast thatwith norepinephrine, its beta
effects are fairly modest.
And what happens here iswhenever you get good blood
pressure support fromnorepinephrine, this normally
happens without that excessiveincrease in your heart rate or a
dramatic increase in yourmyocardial oxygen consumption.
(05:27):
Now, clinically, norepinephrineis oftentimes the first line
agent in septic shock.
Now, in anesthesia, oftentimeswe're leaning more towards maybe
ephedrin or phenyphrine, butmore and more we're using
norepinephrine because of itsbalance effects.
It's gonna help to restore thatperfusion pressure while really
(05:49):
preserving that cardiacefficiency.
Now, whenever you're thinking onthat cRNA level, that more
in-depth level, you're gonna seehow it improves amino arterial
pressure by increasing your SVR.
It's gonna help maintain thatnice balance that we like to
see.
And this is that balance betweenoxygen delivery and then demand.
(06:12):
Now, with norepinephrine,excessive vasoconstriction can
impair that microcirculatoryflow.
So whenever you're thinkingabout getting that mean arterial
pressure higher, you want to seeit correlated with signs of good
tissue perfusion, maybe lactateclearance, uh urinary output to
(06:34):
make sure you have renalperfusion.
But we've all seen how excessiveuse of norepinephrine, all
right, can lead to thatshunting, all right, from your
periphery to your core.
All right.
So whenever you're thinkingabout norepinephrine and
anesthesia, we really enjoy it,especially for our patients with
(06:58):
a decreased ejection fraction.
Whenever I'm setting up for acase and I'm looking at my
patient, I'm doing mypre-anesthetic assessment.
Anybody I see with an EF oftypically less than 30%, I'm
thinking, do I need to grab somenorepinephrine and have it on
hand?
You can also think about,especially whenever you're
wanting to consider what makesthe good CRNA, is that ability
(07:22):
to very quickly do medicationmath.
With that being said, knowinghow to dilute norepinephrine,
oftentimes you're going to seeit come in a couple different
concentrations.
All right.
We normally have fourmilligrams, eight milligrams,
and then sixteen milligrams and250 mls.
So normal single, double, andthen quad strength letho.
(07:44):
Knowing how to dilute those,Dorik can have a push syringe of
norepinephrine aside from yourdrip.
Normally we're pushing somewherebetween 1.6 and 3.2 mics.
All right.
Now let's switch gears a littlebit.
Let's talk about phenylephrin,pure alpha.
We love phenylephrin inanesthesia.
Not a lot of beta activity.
(08:05):
That alpha-1 stimulation that'sgonna cause that intense
arterial and venousvasoconstriction.
With that venous constriction,you're going to get an increase
in venous return initially.
Okay?
But that arterial constrictionincreases after load.
In response to that increasedSVR, you're gonna get activation
(08:28):
of your baroreceptors.
This is gonna lead to thatreflex vagal stimulation and
bradycardia.
Because if phenylephrine doesnot increase contractility,
cardiac output can actuallydecrease despite that improved
amine arterial pressure.
Now, when it comes tophenolephrin, we often have it
(08:49):
uh either pre-drawn in ouranesthesia carts and pre-premix
syringes at typically 100 micsper mil, or you may mix it up
during the during the beginningof the day or beginning of the
case.
Phenolephrin is very, veryuseful in anesthesia.
When you think about increasingthat myocardial oxygen demand
(09:12):
with that increase in a heartrate, we often like
phenolephrine because it's goingto decrease that heart rate.
In patients who are especiallyES both 30% and higher,
phenolephrine is a very usefulagent.
It's not as potent asnorepinephrine, it's a little
bit more forgiving.
Because it increases pressure atthe expense of flow, it's very
(09:32):
appropriate when thathypotension is caused by
vasodilation and your cardiacoutput is already adequate.
Especially useful in healthypatients with anesthetic-induced
hypotension.
Now, when it comes to septicshock in somebody with maybe
impaired cardiac output, thiscan worsen that tissue perfusion
(09:54):
despite a normal mean arterialpressure.
So that's why I mentionedearlier with phenolictrin, we
oftentimes think about how itwill be used and is this patient
able to handle it from acardiovascular standpoint.
So whenever you are thinkingabout that choice of vasopressor
(10:14):
and what your patient's on, lookat do you have an echo?
What valvular issues do theyhave?
Aortic stenosis is one that inan expedition we often talk
about, all right, that can be avery dangerous, dangerous
patient to put to sleep issomebody with severe or critical
aortic stenosis.
We oftentimes like phenylephrinebecause that's going to keep
(10:35):
that heart rate on the lowerside.
Now let's move on and talk alittle bit about vasopressin.
This works through a completelydifferent system.
It acts on your V1 receptors,and that's located on vascular
smooth muscle.
These are G protein coupledreceptors that are activated by
vasopressin.
And remember that vasopressin isthat antidiuretic hormone.
(10:57):
So it's going to mediatevasoconstriction and raise blood
pressure.
And you have some subtypes ofthose V1 receptors, but we
really kind of group thosetogether.
So V1 receptor activation,that's going to uh stimulate
that phospholycase C, and thisleads to that increase in
(11:18):
intracellular calcium levels andthat potent vasoconstriction.
Whenever you were givingvasopressin in the ICU, it's
normally in a drip, inanesthesia, can be in a drip.
Oftentimes we're mixing it upand we're pushing it either and
mixing it up to normally one totwo units per ml, and we're
pushing somewhere between 0.5and 2 units at a time.
(11:40):
Two units is a big dose.
Okay, if I'm mixing a vaso,unless someone is completely
vasoplegic and I need to give abig dose because they're
incredibly hypotensive, I'mnormally starting with a much
smaller dose.
Normally that 0.5 to 1.
So the mechanism of vasopressinis unique because it's
independent of those alpha andbeta receptors.
In septic shock, our endogenousvasopressin levels are initially
(12:04):
elevated and then they depleteover time.
This is thatcatecholamine-resistant
vasodilation.
Vasopressin is going to help torestore that vascular tone
because it bypasses thatadrenergic receptor pathway.
Vasopressin is very useful whensomeone is not responsive to
ephedrin, phenylephrin, allright?
(12:25):
Because it increases your meanarterial pressure without
increasing heart rate orcontractility, it's very useful.
Somebody with maybe a tachyarrhythmia or a limited cardiac
reserve, I mentioned someone whois vasoplegic.
Vasopressin is oftentimes in anas feature we talk about ACE
inhibitor-induced hypotension,maybe post-induction.
Vasopressin is going to be yourgo-to, all right, because it's
(12:48):
acting on a completely differentset of receptors.
So vasopressin maintains thatefficacy even in acidotic
states.
Catecholines lose their receptorsensitivity as someone becomes
more acidotic.
But vasopressin causes thatnon-selective vasoconstriction.
And now, excess dosing, allright, this can reduce blood
(13:10):
flow.
And this can this can betraumatic.
This can be blood flow to thegut, to the skin, to your
cornear circulation.
And that's why in the ICU you'regoing to see it normally as a
fixed dose adjunct.
And it's not aggressively tiedtogether in the anesthesia,
though, especially if thathypotension is certainly
directly related to ouranesthetic drugs short term.
(13:33):
That's why we're able to use itin a IV push standpoint.
So now backing out a little bit,we've talked about
norepinephrine, we've talkedabout phenylephrine, we've
talked about vasopressin.
Some key points here.
That alpha-1 stimulation, that'sgoing to increase your SVR and
your arterial pressure.
That beta 1 stimulation, as yourheart rate goes up, your
(13:55):
contractility, and your cardiacoutput, alpha is going to fix
that pressure, and that betastimulation is going to help to
fix flow.
Your decision-making as a cRNAis going to determine whether
your hypotension and yourknowledge of your patient is
this a vascular tone problem, isthis a cardiac performance
(14:15):
problem?
And when you use alpha agents inlow cardiac output states, this
can worsen organ perfusion.
You have to be very careful.
Using beta-heavy agents, allright, in vasodilatory shock can
worsen that hypotension.
That balance matters.
That's why I talked about thatejection fraction earlier, those
valvular abnormalities, howthose can oftentimes dictate
(14:36):
what pressure we use.
And honestly, those valvulardisorders certainly dictate the
anesthetic choice that we use.
If we can, if we can avoidgeneral anesthesia, we certainly
want to.
(14:57):
Because you're going to havethat dramatic drop in blood
pressure.
So whenever you're thinkingabout your patient and you're
thinking about where do I wantto get their blood pressure,
it's not one single number.
It's not a systolic of this,it's not a diastolic of this,
it's not even a map of this.
Your goal should beindividualized.
(15:19):
You have to think about inanesthesia, positioning is a big
one.
Okay, if I have a patient who'ssitting up doing a shoulder
surgery, okay, I'm wanting tomake sure that the brain is
getting perfused.
If I just shoot for a map of 65and I throw a blood pressure up
anywhere, I may not get goodcerebral perfusion.
All right, patients have hadstrokes, patients have died from
poor cerebral perfusion insitting cases.
(15:40):
So individualize those goals.
Think about your cerebral andyour renal autoregulation.
How this is shifted in patientswho are chronically
hypertensive.
One of the things, and if any ofmy students are listening, one
of the things I say oftentimesis long-acting antihypertensives
(16:01):
have no place in intraoperativeanesthesia.
Okay?
And yet in anesthesia hearts,you're going to see lots of
long-acting antihypertensivestocks, uh libatolol,
mitoprolol, hydrolizine.
Okay?
And sometimes those drugs areused.
But I always challenge people,I've never been in a surgery and
said, I can guarantee no matterwhat happens for the next four
(16:22):
to six hours, I want to lowerblood pressure.
Things can change at any moment,okay?
We like short-acting agents.
So this way, if you give thatlong-acting drug, you're not
having to fight those pooreffects whenever your patient
starts bleeding.
So individualize those goals.
Consider what that patient withchronic hypertension needs.
(16:45):
They don't need to be broughtdown to a blood pressure of 110
over 70.
They may be sitting in therecovery room vomiting for hours
with a splitting headachebecause they are so hypotensive
and they're uh they're used tobeing so much higher.
You know how to type your dripsin the ICU.
You're gonna translate that,okay, to real-time, in the
(17:08):
moment uh uh pushes of avasopressor agent, knowing how
much to give, knowing yourpatient.
It's gonna be a completelydifferent type of management.
But you're building thatfoundation.
We want to see that you know howthese drugs work.
It's more than simply just umturning on a drip, turning off a
(17:29):
drip.
We want to see, as a good ICUnurse, you showing up and
knowing the receptorpathophysiology of these drugs,
knowing when to usephenolephrine, knowing when to
use norepinephrine, knowing whento use vasopressin.
Okay.
Now, some common pitfalls thatyou might find yourself in have
(17:51):
you optimized your patient?
Do they need more preload?
Are they in heart failure?
Do they need diures?
As you improve that meanarterial pressure, this should
give you improved tissueperfusion.
Does their urinary outputincrease?
All right.
If it does not, if that urinaryoutput has dropped and you get
(18:13):
that blood pressure elevated,why is it still low?
What's happening with thatpatient?
Have they had an acute renalinjury?
Has something else happened?
Is there another reason why?
Are they a dialysis patient?
So one thing that you're gonnasee over and over whenever
you're talking to CRAs, whenyou're talking to anesthesia
providers, we are continuallyassessing our patient.
(18:34):
We are thinking about everysingle drug we give, the
positives, the negatives.
We're thinking about how this isgoing to affect the patient in
the moment, and then also afterthat surgery, after that
procedure.
Okay?
So you're gonna use yourvasopressors to uh immediately
(18:54):
augment that loss in vasculartone from our anesthetic agents.
You're going to use the rightvasopressors depending on your
patient.
It it is not a simple recipe ofuse this drug for this patient.
Everything should beindividualized.
All right.
That's a down and dirty goodreview of your vasopressor
(19:16):
agents.
Uh I certainly want to open itup to uh the chat right now to
ask any questions.
Feel free to ask about anythinganesthesia related.
I'll try to scroll up through itand see if um any questions have
been asked.
Otherwise, feel free to throw itin the chat now.
(19:38):
Is anybody applying to schoolright now or have an interview
coming up?
Whenever you think aboutapplying to school, you need,
and I always tell people, thebest things to review are your
ACLS and your PALs, yourcommonly used drugs, and how are
those going to affect yourpatients?
Studying for CCRN is a veryuseful tool as well.
(20:01):
Knowing how to handle thosecritical patients, knowing how
to answer questions related tothat.
Um, why isn't uh nitrogen usedin the indicates to maintain uh
induction before waking up?
So uh so uh nitrous oxide, allright.
Some some anesthesia providersreally like nitrous, okay?
(20:21):
Nitrous is uh quick on, quickoff.
Okay.
70-30 nitrous, the textbookstatement to that, is uh you
know, it's gonna give you someanalgesic control, but nitrous
also has some negative sideeffects.
Okay, there are the short-termside effects that can cause them
nausea.
Some people kind of debate onthat, um, but I I feel like by
(20:43):
far and large, most anesthesiaproviders are gonna see that,
and they're gonna say nitrous uhis still gonna cause some
nausea.
Diffusion hypoxia, it's notreally good for patients who
have COPD or may have blebs orthings like that.
And overall, I think nitrous haskind of fallen out of favor.
We use it in pediatricinductions, but it's quick on,
quick off.
(21:03):
You can turn off your volatileagents, turn off your SIBO, turn
off your DES, and use 7030nitrous, and then very quickly
at the end of the case, justturn up your oxygen and uh
people breathe it off prettyquickly.
Uh someone said, I have appliedin the last two years, we're
going to hear from them in theupcoming months.
Good job.
Certainly keep applying.
(21:25):
As more schools open up, as moreopportunities become available.
Um we certainly need CRNAs rightnow and anticipating future
needs of the profession as well.
So all of our really, reallygood ICP nurses that want to go
this route, I really encourageyou.
CSPA has a ton of tools to uh tohelp you uh move forward.
(21:46):
Um, how would you distinguishthe mechanism of action and the
effects of epi and norepi?
When talking about epinephrineand norepinephrine, okay, or
adrenaline, noradrenaline, withepinephrine, you're going to see
those.
Intense beta effects.
Okay, you're gonna see thatreally, really rapid increase in
heart rate.
You're also gonna see thosealpha effects as well.
(22:06):
Well, norepinephrine, less ofthose beta, all right, a little
bit more alpha.
So an epidrip, okay, oftentimesI'm seeing somebody who has
intense, okay, like uh anepidrip is really, really
useful, and someone who's had ananaphylactic reaction and they
have this huge, all right, thisphase devalatory response, all
right.
We really, really likeepinephrine in those cases.
(22:29):
But if it's somebody who needs avasopressor, maybe somebody with
a reduced ejection fraction, youdon't want to increase that
myocardial oxygen demand sohigh.
Okay?
You don't want to increase thatheart rate so high.
So norepinephrine would probablybe a little bit more useful in
those situations.
Um yeah, so anestheticconsiderations for valvular
(22:50):
conditions.
Simplistically, okay, thesestenotic lesions, okay, we
typically want normal sinusrhythm, we want a low normal
heart rate, all right, and wewant to maintain that pressure.
With your regurgitent lesions,we normally say full, fast, and
forward, okay, plenty ofpreload, keep that heart rate
normal to a little elevated, allright, and then keep things
(23:12):
moving forward.
Now, sometimes you'll have mixedlesions.
You'll have patients that maybehave mild aoridic spinosis and
then moderate to severe mitralregurge.
When you have a patient that hasa mixed lesion, what you want to
consider is the most severe ofthat lesion, which valvular
lesion is the most severe, andthen you're gonna lean towards
that.
(23:32):
Uh a little trick I use iswhat's their baseline blood
pressure heart rate when theycome in?
All right, their heart rate's60, all right, they're
functioning fine, they're notsymptomatic, all right.
Odds are I'm gonna want to keepthat heart rate on the lower
side.
If they come in and theirresting heart rate's 80, 85, all
right, they'd probably dobetter, a little bit more
compensated with a quicker heartrate.
(23:53):
Now, when it comes to thatejection fraction, okay, um I
cared for a patient the otherday who had an EF of 20%, all
right.
The patient's gonna be verysensitive to anesthetic agents,
okay?
They're not gonna toleratehypotension.
So whenever you have a reducedEF, like I said, normally if
it's less than 30%, we wantsomething balanced.
(24:14):
We're not leaved.
We want to maintain that bloodpressure where it is.
We don't want those dropsbecause it's gonna be very, very
hard for that patient tocompensate.
You have to be very, verycareful about the fluids you
give, all right, you know, tothat patient into full CHF, all
right, if you bolt some a coupleliters of fluids.
So in those situations, I'mgonna want to roll into the OR,
(24:35):
have a, you know, I'm talkinglower EF, probably less than
30%, have an arterial line inplace if I'm doing a general
anesthetic, hook it up, or havegive them any medications, see
where they're at.
Go ahead and start my drip if Ihave uh norepia in the room,
phenylephrine.
Whatever I have, I want to goahead and start it because I
know they're gonna droppost-induction.
I don't want them to have aprecipitous drop.
(24:57):
I want a very smooth induction,okay?
So not a not a big bunch ofpropofol, nothing that's gonna
cause a ton of vasodilation.
All right.
Any other questions aboutanything anesthesia related?
These have all been very, verygood.
Um that and that's that is thegreat part about you know
(25:18):
working in ICU.
This gives you such a solidfoundation to uh to move forward
in the profession.
And certainly, like I said, withanesthesia, we have a great need
right now, and we're gonnaanticipate even more moving
forward.
Uh cardion shining, my patientcame up on cardine after a heart
transplant on a balloon bone, hegets hypertensive and on cardine
(25:39):
to prevent balloon rupture.
Uh heard dropping is SATS.
Um Yeah, that's a that's a veryuh compli that's a very
complicated case.
I think it's gonna depend onwhere that patient was to begin
with.
Um I don't use cardian a ton.
Um I'm very much, you know, ifI'm using uh you know
(25:59):
antihypertensives, short acting,esmalol, uh nitro.
But more than likely on thatpatient, wanted to get that
pressure down and um droppinghis stats.
Maybe something else going on inthere, but certainly cardine can
have some of those negativeeffects as well.
Um yeah, I've used uh uhGeopreza or was it angiotensin
(26:22):
II in the OR.
Normally it's gonna come as adrip.
And I think if I remembercorrectly, um angiotensin II,
it's actually more effective ifsomebody has been on an ACE
inhibitor, or it can be veryeffective.
So we don't use it as I've neverused it as a push, some people
might.
I I doubt it, but I know it's Iknow it's expensive, I know it's
(26:43):
you know newer-ish and is very,very useful.
I you know, like I said, havebrought patients down to the OR
with it and normally justmaintain at whatever rate it's
going at.
Uh yeah, some examples of someinterview questions.
So I I think a very softballquestion.
Normally you're gonna be askedby everybody, why do you want to
be a CRNA?
And that should be a veryindividualized response.
(27:06):
Why do you want to be a CRNA?
And how maybe your firstinteraction, you want to give a
very genuine response.
Uh from there, when we askclinical questions, in my
personal opinion, I think thebest clinical questions to ask
are questions you could askevery good ICU nurse.
So ACLS, PALS, BLS, you know, ifwe ask you how a drug works,
(27:29):
what's your, you know, you comeinto a patient's room and I've
shown people EKGs before, youknow, simple kind of the
textbook rhythms, um, and thenkind of ask them their response.
Because I want to see, can youthink independently?
Are you very are you tooprotocol-based?
Are you so used to callingorders that you can't think
outside the box?
I want to see people who arewanting to understand the full
(27:50):
picture, who don't tell me, oh,we follow this protocol and do
this.
But why do you do that?
All right.
Uh how many doses of ephedrinedo you get before you reach for
alternatives beside the usual uhneo uh or so like with ephedrin,
I'm probab honestly a dose ortwo, unless somebody is uh, like
(28:11):
I said, um very redocardic and Idon't want to give any more
phenylephrine, and then veryquickly I'm probably gonna call
for if I don't have norepia inthe room to mix it, um, call for
something.
I've seen some people give likeglycopyroate to get the heart
rate up.
I've seen people try to usepolypharmacy to where they can
then use their pressure ofchoice, but very quickly you'll
(28:32):
see the tachyclaxis withephedrin.
Uh one of the old school thingsto do with ephedrin is to do iam
ephedrin, especially uh with a Csection, you put it in your
spinal, give them some Iamephedrin.
And uh, you know, that worksvery, very well.
I will say for the most part,uhphedrin use in OB.
We've 15 years ago, umphenolethrin was rarely used in
(28:52):
OB, and now it's used more andmore.
We use neodrips in C-sectionsnow.
Ephedrin causes phetal acidosis,phenylethrin is gonna cause
fetal brachicardia.
We're still looking for thatbalance in those agents.
For me, two, three doses ofephedrin, sometimes most places
I work have pre-mixed sticks.
If I go through 25 milligrams,all right, I'm gonna switch to
(29:12):
something else.
All right.
Um yeah, so ketamine is veryuseful.
Uh ketamine, in somebody withmaybe severe pulmonary
hypertension, ketamine can helpaugment that a little bit.
I did a TE the other day andused uh just a Scotia ketamine,
25 milligrams to help augmentthis patient with very, very
sick, reduced injectionfraction, valvular issues.
(29:32):
Um it was a regurgitent leasing,not a stenotic one, because
ketamine can cause a littleincrease in that heart rate.
Very, very useful.
The downsides to ketamine, thedysphoria.
All right, patients don't feelthemselves.
unknown (29:46):
All right.
Dr. Harmon (29:46):
Ketamine is also one of those drugs, if you give it
in a multimodal approach, it canbe very useful.
But if anything goes wrong, ifthe patient is not acting right
in the recovery room, it's thefirst drug you blame.
So whenever you're usingketamine, I always recommend
having a very good reason to useit, all right, and don't just
give it, you know, to everysingle patient every single
(30:08):
time.
Because if you can'tindependently assess its
effects, it's going to be hardto say, okay, hey, this is my
go-to drug.
Um I've seen ketamine given inthe recovery room before, and
patients have some not so good,uh not so good effects.
All right.
Um the difference between uhnicotinic muscularic receptors,
opioid receptors, uh mu1 kappa.
(30:30):
So uh two different things.
Whenever you're thinking aboutyour nicotinic and your
muscronic receptors, that'sgonna be talking more about your
neuromuscular blockers and thatpathophysiology, your opioid
receptors, um mu, kappa, delta.
Those are gonna be geared moretowards uh drugs like fentanyl,
morphine, things like that.
(30:50):
Certainly with anesthesia, and Icould do a a whole lecture on
that.
You're gonna get into uh such anin-depth understanding of those
receptors and how they uh relateto our drugs.
How to prepare for thesimulation portion and research
analysis uh portion of aninterview.
Uh practice, practice, practice.
Uh if you're a member of CSPA,we have lots of uh lectures over
(31:14):
the interview, we have infosessions, we have some just, you
know, meet for an hour and kindof let the audience take us
wherever we want to to askquestions.
But if you're not signed up, notin, um not able to attend those,
research, talk to people, findsomebody that you can practice
with, that's the uh the bestway.
(31:35):
What about sedation, volatileinfusion considerations with
cardiac disease, valvularcardiomyopathy, low EF?
Really just depends on thepatient.
You have to be very careful withsedation.
Um certainly don't want toover-sedate people uh with our
volatile anesthetics.
You know, normally quick on,quick off, desflurane, but that
can, you know, high doses cancause tachycardia.
(31:57):
Um, you know, in cardiacsurgeries, there are places that
are still, you know, using ISO,SIVO is very common.
Some are doing more of a TiVwith a little bit of gas.
But the big thing is gonna bemaintaining their blood pressure
at their baseline, not droppingit, and not over-anesthetizing
someone.
Okay.
(32:17):
All right, and then I'll do onemore question or we can recap.
When it comes to preparing foran interview or thinking about
uh going to CRNA school, youwant to be a top-notch IC nurse.
(32:39):
Okay.
That doesn't mean you need 10years of IC experience, okay?
But you need a good solid atminimum a year to start
applying, and then you'll havetwo, two and a half years by the
time you start taking care ofvery sick patients.
This way, whenever youtransition into the OR, you're
used to a lot of these drugs.
You're used to dealing withpatients who are incredibly
(33:02):
unstable.
All right.
Most general anestheticsshouldn't be like that.
But you're gonna the mostunstable critical patient you've
ever had at bedside, you'll haveso much more in the operating
room.
You'll have so much moreresponsibility.
So really solidifying yourfoundation, learning as much as
you can about these drugs, andgetting that really good
experience, taking care of thosesuper sick patients, is going to
(33:24):
help prepare you for thattransition and that role into
being an anesthesia provider.
All right.
I've really enjoyed this.
Uh got to ask a bunch of peoplehave to ask a bunch of good
questions.
Uh don't forget to check out ourwebsite at CRNA School Crep
Academy.com.
Come to our Louisvilleconference in June, and uh
remember to check out uh ourlink tree.
(33:47):
We've got a great uh communityon Circle.
And by all means, you know, ifif you're not a member yet,
consider joining.
We have info sessions uh acouple times a week, and you'll
get a lot of valuable, uhvaluable resources as you're
looking to apply and go to CRNASchool.
Awesome.
Thank you all very much.
(34:07):
Have a wonderful rest of yourday.
Jenny Finnell (34:10):
Thank you for joining us on the Sierra Nation
School Prep Academy podcast.
We hope today's episode gave youclarity and confidence for the
road ahead.
Keep showing up for your goals,keep learning, and keep
believing what's possible foryou.
We're always rooting for you inyour future as a CRNA.
Until next time, take care.
Welcome to the CRM School Park Family Comcast,
where we have helped combinemore than 10,000 IC nurses on
their path towards CRMA school.
Our mission is to combineeducation, guidance, and
professional health so you canmove comfortably towards your
dream of becoming a CRMA.
Whether you're still a nursingschool or a seasoned IC nurse.
This podcast is here for you.
(00:21):
Let's get into today's episode.
Welcome back to Cyrus CoverAcademy Podcast.
Today you're listening to one ofour faculty web sessions, stream
live on CSPA's Instagram.
Depend on the day, this may bean open QA where we take your
questions in real time or afocus company discussion where
we go deep on the area that canstrengthen your knowledge and
build your confidence.
If you want to follow along,join us live, make sure to
(00:42):
follow CSPA on Instagram andwatch for session announcements.
You can also join CSPA's freecommunity where we'll share the
schedule of upcoming sessions.
When you tune in live, you canask questions, get clarity on
the spot, and then learnalongside other nurses
navigating the same path.
And as a quick reminder aboutwho you're learning from, every
session is led by CSPA coachesand faculty who are deeply
committed to your success inpursuing this career.
(01:04):
Without further ado, let's getinto today's show.
Dr. Harmon (01:08):
Hello, everybody.
My name is Dr.
Matthew Harmon.
I'm one of the faculty coacheswith CSPA.
I've got almost nine yearsexperience as a CRNA and have
been in academia for the lastfive and a half, almost six
years.
So today we're going to do avasopressor review.
(01:29):
We're going to go ahead and lookat some principles on
vasopressor usage, some thingsyou need to know whenever you're
thinking about CRNA school.
And then we'll open it up for alittle Q ⁇ A here in just a
little bit.
But before we do, I want toremind everybody, we have our
live conference, uh in-personconference for CSPA in
(01:50):
Louisville, Kentucky in June.
So check check that out and viewour free community via the link
tree in our bio.
So when it comes to choosing theright agent or the right
vasopressor, you need to thinkabout the principles you know as
an ICU nurse.
And then also you need to thinkabout what you may need to know
(02:11):
when it comes time for yourinterview.
So you type rate and you usevasopressors every day.
What we want to see in the cRNAworld is that you understand the
receptor pharmacology, thevascular pathophysiology, and
the hemodynamic responses andexpected responses of each drug.
(02:33):
We're going to talk aboutnorepine, phenolephrine, and
vasopressin, and really how thedifferent alpha and beta
receptors translate into realphysiologic effects.
So think about the hemodynamicframework here.
Think about mean arterialpressure.
It's determined by cardiacoutput and times systemic
vascular resistance.
(02:54):
So MAP is going to equal cardiacoutput times SVR.
When you think about cardiacoutput, that's going to be heart
rate multiplied by strokevolume.
Now, stroke volume is going todepend on your preload, your
contractility, and yourafterload.
When we think about hypotension,especially in anesthesia, and
and truthfully, septic shock aswell, this is going to be caused
(03:16):
by that pathophysiologicvasodilation.
This is from inflammatorymediators, and oftentimes our
anesthetic agents cause thatphysiologic vasodilation.
This can lead to a drop in ourSVR.
And this can be sometimesprofound, depending on if the
patient is hypopholemic,positioning in anesthesia, uh
(03:38):
venous pooling.
So vasopressors, by far andlarge, they work to restore that
vascular tone.
Okay?
When you think of restoringintravascular volume, that's
going to be more akin to uhcrystalloids, uh, maybe some
larger colloids as well.
But for our vasopressor agents,we're thinking vascular tone.
(03:59):
Let's really start looking atthe one that most people are
familiar with that you probablyuse every single day, and that's
gonna be norepinephrine.
Norepinephrine has very strongalpha-1 agonism and some mild
beta-1 agonism.
Oftentimes in anesthesia, wethink of norepinephrine as the
more balanced of our vasopressoragents.
(04:22):
So, alpha-1 receptor activation,this is gonna cause that smooth
muscle contraction.
And this is by thatintracellular calcium, as it
increases in that vascularsmooth muscle, those vascular
smooth muscle cells.
This is gonna lead tovasoconstriction, an increase in
your SVR, and an increase inyour MAP.
(04:43):
Now, that beta-1 stimulation,this increases your uh cyclic
AMP and those caritic myocytes.
This leads to that calciuminflux, and this is going to
enhance or augment thatmyocardial contractility.
In anesthesia, whenever you'recoming off of bypass and you're
wanting to enhance thatmyocardial contractility,
oftentimes we're using calcium.
(05:06):
So whenever you contrast thatwith norepinephrine, its beta
effects are fairly modest.
And what happens here iswhenever you get good blood
pressure support fromnorepinephrine, this normally
happens without that excessiveincrease in your heart rate or a
dramatic increase in yourmyocardial oxygen consumption.
(05:27):
Now, clinically, norepinephrineis oftentimes the first line
agent in septic shock.
Now, in anesthesia, oftentimeswe're leaning more towards maybe
ephedrin or phenyphrine, butmore and more we're using
norepinephrine because of itsbalance effects.
It's gonna help to restore thatperfusion pressure while really
(05:49):
preserving that cardiacefficiency.
Now, whenever you're thinking onthat cRNA level, that more
in-depth level, you're gonna seehow it improves amino arterial
pressure by increasing your SVR.
It's gonna help maintain thatnice balance that we like to
see.
And this is that balance betweenoxygen delivery and then demand.
(06:12):
Now, with norepinephrine,excessive vasoconstriction can
impair that microcirculatoryflow.
So whenever you're thinkingabout getting that mean arterial
pressure higher, you want to seeit correlated with signs of good
tissue perfusion, maybe lactateclearance, uh urinary output to
(06:34):
make sure you have renalperfusion.
But we've all seen how excessiveuse of norepinephrine, all
right, can lead to thatshunting, all right, from your
periphery to your core.
All right.
So whenever you're thinkingabout norepinephrine and
anesthesia, we really enjoy it,especially for our patients with
(06:58):
a decreased ejection fraction.
Whenever I'm setting up for acase and I'm looking at my
patient, I'm doing mypre-anesthetic assessment.
Anybody I see with an EF oftypically less than 30%, I'm
thinking, do I need to grab somenorepinephrine and have it on
hand?
You can also think about,especially whenever you're
wanting to consider what makesthe good CRNA, is that ability
(07:22):
to very quickly do medicationmath.
With that being said, knowinghow to dilute norepinephrine,
oftentimes you're going to seeit come in a couple different
concentrations.
All right.
We normally have fourmilligrams, eight milligrams,
and then sixteen milligrams and250 mls.
So normal single, double, andthen quad strength letho.
(07:44):
Knowing how to dilute those,Dorik can have a push syringe of
norepinephrine aside from yourdrip.
Normally we're pushing somewherebetween 1.6 and 3.2 mics.
All right.
Now let's switch gears a littlebit.
Let's talk about phenylephrin,pure alpha.
We love phenylephrin inanesthesia.
Not a lot of beta activity.
(08:05):
That alpha-1 stimulation that'sgonna cause that intense
arterial and venousvasoconstriction.
With that venous constriction,you're going to get an increase
in venous return initially.
Okay?
But that arterial constrictionincreases after load.
In response to that increasedSVR, you're gonna get activation
(08:28):
of your baroreceptors.
This is gonna lead to thatreflex vagal stimulation and
bradycardia.
Because if phenylephrine doesnot increase contractility,
cardiac output can actuallydecrease despite that improved
amine arterial pressure.
Now, when it comes tophenolephrin, we often have it
(08:49):
uh either pre-drawn in ouranesthesia carts and pre-premix
syringes at typically 100 micsper mil, or you may mix it up
during the during the beginningof the day or beginning of the
case.
Phenolephrin is very, veryuseful in anesthesia.
When you think about increasingthat myocardial oxygen demand
(09:12):
with that increase in a heartrate, we often like
phenolephrine because it's goingto decrease that heart rate.
In patients who are especiallyES both 30% and higher,
phenolephrine is a very usefulagent.
It's not as potent asnorepinephrine, it's a little
bit more forgiving.
Because it increases pressure atthe expense of flow, it's very
(09:32):
appropriate when thathypotension is caused by
vasodilation and your cardiacoutput is already adequate.
Especially useful in healthypatients with anesthetic-induced
hypotension.
Now, when it comes to septicshock in somebody with maybe
impaired cardiac output, thiscan worsen that tissue perfusion
(09:54):
despite a normal mean arterialpressure.
So that's why I mentionedearlier with phenolictrin, we
oftentimes think about how itwill be used and is this patient
able to handle it from acardiovascular standpoint.
So whenever you are thinkingabout that choice of vasopressor
(10:14):
and what your patient's on, lookat do you have an echo?
What valvular issues do theyhave?
Aortic stenosis is one that inan expedition we often talk
about, all right, that can be avery dangerous, dangerous
patient to put to sleep issomebody with severe or critical
aortic stenosis.
We oftentimes like phenylephrinebecause that's going to keep
(10:35):
that heart rate on the lowerside.
Now let's move on and talk alittle bit about vasopressin.
This works through a completelydifferent system.
It acts on your V1 receptors,and that's located on vascular
smooth muscle.
These are G protein coupledreceptors that are activated by
vasopressin.
And remember that vasopressin isthat antidiuretic hormone.
(10:57):
So it's going to mediatevasoconstriction and raise blood
pressure.
And you have some subtypes ofthose V1 receptors, but we
really kind of group thosetogether.
So V1 receptor activation,that's going to uh stimulate
that phospholycase C, and thisleads to that increase in
(11:18):
intracellular calcium levels andthat potent vasoconstriction.
Whenever you were givingvasopressin in the ICU, it's
normally in a drip, inanesthesia, can be in a drip.
Oftentimes we're mixing it upand we're pushing it either and
mixing it up to normally one totwo units per ml, and we're
pushing somewhere between 0.5and 2 units at a time.
(11:40):
Two units is a big dose.
Okay, if I'm mixing a vaso,unless someone is completely
vasoplegic and I need to give abig dose because they're
incredibly hypotensive, I'mnormally starting with a much
smaller dose.
Normally that 0.5 to 1.
So the mechanism of vasopressinis unique because it's
independent of those alpha andbeta receptors.
In septic shock, our endogenousvasopressin levels are initially
(12:04):
elevated and then they depleteover time.
This is thatcatecholamine-resistant
vasodilation.
Vasopressin is going to help torestore that vascular tone
because it bypasses thatadrenergic receptor pathway.
Vasopressin is very useful whensomeone is not responsive to
ephedrin, phenylephrin, allright?
(12:25):
Because it increases your meanarterial pressure without
increasing heart rate orcontractility, it's very useful.
Somebody with maybe a tachyarrhythmia or a limited cardiac
reserve, I mentioned someone whois vasoplegic.
Vasopressin is oftentimes in anas feature we talk about ACE
inhibitor-induced hypotension,maybe post-induction.
Vasopressin is going to be yourgo-to, all right, because it's
(12:48):
acting on a completely differentset of receptors.
So vasopressin maintains thatefficacy even in acidotic
states.
Catecholines lose their receptorsensitivity as someone becomes
more acidotic.
But vasopressin causes thatnon-selective vasoconstriction.
And now, excess dosing, allright, this can reduce blood
(13:10):
flow.
And this can this can betraumatic.
This can be blood flow to thegut, to the skin, to your
cornear circulation.
And that's why in the ICU you'regoing to see it normally as a
fixed dose adjunct.
And it's not aggressively tiedtogether in the anesthesia,
though, especially if thathypotension is certainly
directly related to ouranesthetic drugs short term.
(13:33):
That's why we're able to use itin a IV push standpoint.
So now backing out a little bit,we've talked about
norepinephrine, we've talkedabout phenylephrine, we've
talked about vasopressin.
Some key points here.
That alpha-1 stimulation, that'sgoing to increase your SVR and
your arterial pressure.
That beta 1 stimulation, as yourheart rate goes up, your
(13:55):
contractility, and your cardiacoutput, alpha is going to fix
that pressure, and that betastimulation is going to help to
fix flow.
Your decision-making as a cRNAis going to determine whether
your hypotension and yourknowledge of your patient is
this a vascular tone problem, isthis a cardiac performance
(14:15):
problem?
And when you use alpha agents inlow cardiac output states, this
can worsen organ perfusion.
You have to be very careful.
Using beta-heavy agents, allright, in vasodilatory shock can
worsen that hypotension.
That balance matters.
That's why I talked about thatejection fraction earlier, those
valvular abnormalities, howthose can oftentimes dictate
(14:36):
what pressure we use.
And honestly, those valvulardisorders certainly dictate the
anesthetic choice that we use.
If we can, if we can avoidgeneral anesthesia, we certainly
want to.
(14:57):
Because you're going to havethat dramatic drop in blood
pressure.
So whenever you're thinkingabout your patient and you're
thinking about where do I wantto get their blood pressure,
it's not one single number.
It's not a systolic of this,it's not a diastolic of this,
it's not even a map of this.
Your goal should beindividualized.
(15:19):
You have to think about inanesthesia, positioning is a big
one.
Okay, if I have a patient who'ssitting up doing a shoulder
surgery, okay, I'm wanting tomake sure that the brain is
getting perfused.
If I just shoot for a map of 65and I throw a blood pressure up
anywhere, I may not get goodcerebral perfusion.
All right, patients have hadstrokes, patients have died from
poor cerebral perfusion insitting cases.
(15:40):
So individualize those goals.
Think about your cerebral andyour renal autoregulation.
How this is shifted in patientswho are chronically
hypertensive.
One of the things, and if any ofmy students are listening, one
of the things I say oftentimesis long-acting antihypertensives
(16:01):
have no place in intraoperativeanesthesia.
Okay?
And yet in anesthesia hearts,you're going to see lots of
long-acting antihypertensivestocks, uh libatolol,
mitoprolol, hydrolizine.
Okay?
And sometimes those drugs areused.
But I always challenge people,I've never been in a surgery and
said, I can guarantee no matterwhat happens for the next four
(16:22):
to six hours, I want to lowerblood pressure.
Things can change at any moment,okay?
We like short-acting agents.
So this way, if you give thatlong-acting drug, you're not
having to fight those pooreffects whenever your patient
starts bleeding.
So individualize those goals.
Consider what that patient withchronic hypertension needs.
(16:45):
They don't need to be broughtdown to a blood pressure of 110
over 70.
They may be sitting in therecovery room vomiting for hours
with a splitting headachebecause they are so hypotensive
and they're uh they're used tobeing so much higher.
You know how to type your dripsin the ICU.
You're gonna translate that,okay, to real-time, in the
(17:08):
moment uh uh pushes of avasopressor agent, knowing how
much to give, knowing yourpatient.
It's gonna be a completelydifferent type of management.
But you're building thatfoundation.
We want to see that you know howthese drugs work.
It's more than simply just umturning on a drip, turning off a
(17:29):
drip.
We want to see, as a good ICUnurse, you showing up and
knowing the receptorpathophysiology of these drugs,
knowing when to usephenolephrine, knowing when to
use norepinephrine, knowing whento use vasopressin.
Okay.
Now, some common pitfalls thatyou might find yourself in have
(17:51):
you optimized your patient?
Do they need more preload?
Are they in heart failure?
Do they need diures?
As you improve that meanarterial pressure, this should
give you improved tissueperfusion.
Does their urinary outputincrease?
All right.
If it does not, if that urinaryoutput has dropped and you get
(18:13):
that blood pressure elevated,why is it still low?
What's happening with thatpatient?
Have they had an acute renalinjury?
Has something else happened?
Is there another reason why?
Are they a dialysis patient?
So one thing that you're gonnasee over and over whenever
you're talking to CRAs, whenyou're talking to anesthesia
providers, we are continuallyassessing our patient.
(18:34):
We are thinking about everysingle drug we give, the
positives, the negatives.
We're thinking about how this isgoing to affect the patient in
the moment, and then also afterthat surgery, after that
procedure.
Okay?
So you're gonna use yourvasopressors to uh immediately
(18:54):
augment that loss in vasculartone from our anesthetic agents.
You're going to use the rightvasopressors depending on your
patient.
It it is not a simple recipe ofuse this drug for this patient.
Everything should beindividualized.
All right.
That's a down and dirty goodreview of your vasopressor
(19:16):
agents.
Uh I certainly want to open itup to uh the chat right now to
ask any questions.
Feel free to ask about anythinganesthesia related.
I'll try to scroll up through itand see if um any questions have
been asked.
Otherwise, feel free to throw itin the chat now.
(19:38):
Is anybody applying to schoolright now or have an interview
coming up?
Whenever you think aboutapplying to school, you need,
and I always tell people, thebest things to review are your
ACLS and your PALs, yourcommonly used drugs, and how are
those going to affect yourpatients?
Studying for CCRN is a veryuseful tool as well.
(20:01):
Knowing how to handle thosecritical patients, knowing how
to answer questions related tothat.
Um, why isn't uh nitrogen usedin the indicates to maintain uh
induction before waking up?
So uh so uh nitrous oxide, allright.
Some some anesthesia providersreally like nitrous, okay?
(20:21):
Nitrous is uh quick on, quickoff.
Okay.
70-30 nitrous, the textbookstatement to that, is uh you
know, it's gonna give you someanalgesic control, but nitrous
also has some negative sideeffects.
Okay, there are the short-termside effects that can cause them
nausea.
Some people kind of debate onthat, um, but I I feel like by
(20:43):
far and large, most anesthesiaproviders are gonna see that,
and they're gonna say nitrous uhis still gonna cause some
nausea.
Diffusion hypoxia, it's notreally good for patients who
have COPD or may have blebs orthings like that.
And overall, I think nitrous haskind of fallen out of favor.
We use it in pediatricinductions, but it's quick on,
quick off.
(21:03):
You can turn off your volatileagents, turn off your SIBO, turn
off your DES, and use 7030nitrous, and then very quickly
at the end of the case, justturn up your oxygen and uh
people breathe it off prettyquickly.
Uh someone said, I have appliedin the last two years, we're
going to hear from them in theupcoming months.
Good job.
Certainly keep applying.
(21:25):
As more schools open up, as moreopportunities become available.
Um we certainly need CRNAs rightnow and anticipating future
needs of the profession as well.
So all of our really, reallygood ICP nurses that want to go
this route, I really encourageyou.
CSPA has a ton of tools to uh tohelp you uh move forward.
(21:46):
Um, how would you distinguishthe mechanism of action and the
effects of epi and norepi?
When talking about epinephrineand norepinephrine, okay, or
adrenaline, noradrenaline, withepinephrine, you're going to see
those.
Intense beta effects.
Okay, you're gonna see thatreally, really rapid increase in
heart rate.
You're also gonna see thosealpha effects as well.
(22:06):
Well, norepinephrine, less ofthose beta, all right, a little
bit more alpha.
So an epidrip, okay, oftentimesI'm seeing somebody who has
intense, okay, like uh anepidrip is really, really
useful, and someone who's had ananaphylactic reaction and they
have this huge, all right, thisphase devalatory response, all
right.
We really, really likeepinephrine in those cases.
(22:29):
But if it's somebody who needs avasopressor, maybe somebody with
a reduced ejection fraction, youdon't want to increase that
myocardial oxygen demand sohigh.
Okay?
You don't want to increase thatheart rate so high.
So norepinephrine would probablybe a little bit more useful in
those situations.
Um yeah, so anestheticconsiderations for valvular
(22:50):
conditions.
Simplistically, okay, thesestenotic lesions, okay, we
typically want normal sinusrhythm, we want a low normal
heart rate, all right, and wewant to maintain that pressure.
With your regurgitent lesions,we normally say full, fast, and
forward, okay, plenty ofpreload, keep that heart rate
normal to a little elevated, allright, and then keep things
(23:12):
moving forward.
Now, sometimes you'll have mixedlesions.
You'll have patients that maybehave mild aoridic spinosis and
then moderate to severe mitralregurge.
When you have a patient that hasa mixed lesion, what you want to
consider is the most severe ofthat lesion, which valvular
lesion is the most severe, andthen you're gonna lean towards
that.
(23:32):
Uh a little trick I use iswhat's their baseline blood
pressure heart rate when theycome in?
All right, their heart rate's60, all right, they're
functioning fine, they're notsymptomatic, all right.
Odds are I'm gonna want to keepthat heart rate on the lower
side.
If they come in and theirresting heart rate's 80, 85, all
right, they'd probably dobetter, a little bit more
compensated with a quicker heartrate.
(23:53):
Now, when it comes to thatejection fraction, okay, um I
cared for a patient the otherday who had an EF of 20%, all
right.
The patient's gonna be verysensitive to anesthetic agents,
okay?
They're not gonna toleratehypotension.
So whenever you have a reducedEF, like I said, normally if
it's less than 30%, we wantsomething balanced.
(24:14):
We're not leaved.
We want to maintain that bloodpressure where it is.
We don't want those dropsbecause it's gonna be very, very
hard for that patient tocompensate.
You have to be very, verycareful about the fluids you
give, all right, you know, tothat patient into full CHF, all
right, if you bolt some a coupleliters of fluids.
So in those situations, I'mgonna want to roll into the OR,
(24:35):
have a, you know, I'm talkinglower EF, probably less than
30%, have an arterial line inplace if I'm doing a general
anesthetic, hook it up, or havegive them any medications, see
where they're at.
Go ahead and start my drip if Ihave uh norepia in the room,
phenylephrine.
Whatever I have, I want to goahead and start it because I
know they're gonna droppost-induction.
I don't want them to have aprecipitous drop.
(24:57):
I want a very smooth induction,okay?
So not a not a big bunch ofpropofol, nothing that's gonna
cause a ton of vasodilation.
All right.
Any other questions aboutanything anesthesia related?
These have all been very, verygood.
Um that and that's that is thegreat part about you know
(25:18):
working in ICU.
This gives you such a solidfoundation to uh to move forward
in the profession.
And certainly, like I said, withanesthesia, we have a great need
right now, and we're gonnaanticipate even more moving
forward.
Uh cardion shining, my patientcame up on cardine after a heart
transplant on a balloon bone, hegets hypertensive and on cardine
(25:39):
to prevent balloon rupture.
Uh heard dropping is SATS.
Um Yeah, that's a that's a veryuh compli that's a very
complicated case.
I think it's gonna depend onwhere that patient was to begin
with.
Um I don't use cardian a ton.
Um I'm very much, you know, ifI'm using uh you know
(25:59):
antihypertensives, short acting,esmalol, uh nitro.
But more than likely on thatpatient, wanted to get that
pressure down and um droppinghis stats.
Maybe something else going on inthere, but certainly cardine can
have some of those negativeeffects as well.
Um yeah, I've used uh uhGeopreza or was it angiotensin
(26:22):
II in the OR.
Normally it's gonna come as adrip.
And I think if I remembercorrectly, um angiotensin II,
it's actually more effective ifsomebody has been on an ACE
inhibitor, or it can be veryeffective.
So we don't use it as I've neverused it as a push, some people
might.
I I doubt it, but I know it's Iknow it's expensive, I know it's
(26:43):
you know newer-ish and is very,very useful.
I you know, like I said, havebrought patients down to the OR
with it and normally justmaintain at whatever rate it's
going at.
Uh yeah, some examples of someinterview questions.
So I I think a very softballquestion.
Normally you're gonna be askedby everybody, why do you want to
be a CRNA?
And that should be a veryindividualized response.
(27:06):
Why do you want to be a CRNA?
And how maybe your firstinteraction, you want to give a
very genuine response.
Uh from there, when we askclinical questions, in my
personal opinion, I think thebest clinical questions to ask
are questions you could askevery good ICU nurse.
So ACLS, PALS, BLS, you know, ifwe ask you how a drug works,
(27:29):
what's your, you know, you comeinto a patient's room and I've
shown people EKGs before, youknow, simple kind of the
textbook rhythms, um, and thenkind of ask them their response.
Because I want to see, can youthink independently?
Are you very are you tooprotocol-based?
Are you so used to callingorders that you can't think
outside the box?
I want to see people who arewanting to understand the full
(27:50):
picture, who don't tell me, oh,we follow this protocol and do
this.
But why do you do that?
All right.
Uh how many doses of ephedrinedo you get before you reach for
alternatives beside the usual uhneo uh or so like with ephedrin,
I'm probab honestly a dose ortwo, unless somebody is uh, like
(28:11):
I said, um very redocardic and Idon't want to give any more
phenylephrine, and then veryquickly I'm probably gonna call
for if I don't have norepia inthe room to mix it, um, call for
something.
I've seen some people give likeglycopyroate to get the heart
rate up.
I've seen people try to usepolypharmacy to where they can
then use their pressure ofchoice, but very quickly you'll
(28:32):
see the tachyclaxis withephedrin.
Uh one of the old school thingsto do with ephedrin is to do iam
ephedrin, especially uh with a Csection, you put it in your
spinal, give them some Iamephedrin.
And uh, you know, that worksvery, very well.
I will say for the most part,uhphedrin use in OB.
We've 15 years ago, umphenolethrin was rarely used in
(28:52):
OB, and now it's used more andmore.
We use neodrips in C-sectionsnow.
Ephedrin causes phetal acidosis,phenylethrin is gonna cause
fetal brachicardia.
We're still looking for thatbalance in those agents.
For me, two, three doses ofephedrin, sometimes most places
I work have pre-mixed sticks.
If I go through 25 milligrams,all right, I'm gonna switch to
(29:12):
something else.
All right.
Um yeah, so ketamine is veryuseful.
Uh ketamine, in somebody withmaybe severe pulmonary
hypertension, ketamine can helpaugment that a little bit.
I did a TE the other day andused uh just a Scotia ketamine,
25 milligrams to help augmentthis patient with very, very
sick, reduced injectionfraction, valvular issues.
(29:32):
Um it was a regurgitent leasing,not a stenotic one, because
ketamine can cause a littleincrease in that heart rate.
Very, very useful.
The downsides to ketamine, thedysphoria.
All right, patients don't feelthemselves.
unknown (29:46):
All right.
Dr. Harmon (29:46):
Ketamine is also one of those drugs, if you give it
in a multimodal approach, it canbe very useful.
But if anything goes wrong, ifthe patient is not acting right
in the recovery room, it's thefirst drug you blame.
So whenever you're usingketamine, I always recommend
having a very good reason to useit, all right, and don't just
give it, you know, to everysingle patient every single
(30:08):
time.
Because if you can'tindependently assess its
effects, it's going to be hardto say, okay, hey, this is my
go-to drug.
Um I've seen ketamine given inthe recovery room before, and
patients have some not so good,uh not so good effects.
All right.
Um the difference between uhnicotinic muscularic receptors,
opioid receptors, uh mu1 kappa.
(30:30):
So uh two different things.
Whenever you're thinking aboutyour nicotinic and your
muscronic receptors, that'sgonna be talking more about your
neuromuscular blockers and thatpathophysiology, your opioid
receptors, um mu, kappa, delta.
Those are gonna be geared moretowards uh drugs like fentanyl,
morphine, things like that.
(30:50):
Certainly with anesthesia, and Icould do a a whole lecture on
that.
You're gonna get into uh such anin-depth understanding of those
receptors and how they uh relateto our drugs.
How to prepare for thesimulation portion and research
analysis uh portion of aninterview.
Uh practice, practice, practice.
Uh if you're a member of CSPA,we have lots of uh lectures over
(31:14):
the interview, we have infosessions, we have some just, you
know, meet for an hour and kindof let the audience take us
wherever we want to to askquestions.
But if you're not signed up, notin, um not able to attend those,
research, talk to people, findsomebody that you can practice
with, that's the uh the bestway.
(31:35):
What about sedation, volatileinfusion considerations with
cardiac disease, valvularcardiomyopathy, low EF?
Really just depends on thepatient.
You have to be very careful withsedation.
Um certainly don't want toover-sedate people uh with our
volatile anesthetics.
You know, normally quick on,quick off, desflurane, but that
can, you know, high doses cancause tachycardia.
(31:57):
Um, you know, in cardiacsurgeries, there are places that
are still, you know, using ISO,SIVO is very common.
Some are doing more of a TiVwith a little bit of gas.
But the big thing is gonna bemaintaining their blood pressure
at their baseline, not droppingit, and not over-anesthetizing
someone.
Okay.
(32:17):
All right, and then I'll do onemore question or we can recap.
When it comes to preparing foran interview or thinking about
uh going to CRNA school, youwant to be a top-notch IC nurse.
(32:39):
Okay.
That doesn't mean you need 10years of IC experience, okay?
But you need a good solid atminimum a year to start
applying, and then you'll havetwo, two and a half years by the
time you start taking care ofvery sick patients.
This way, whenever youtransition into the OR, you're
used to a lot of these drugs.
You're used to dealing withpatients who are incredibly
(33:02):
unstable.
All right.
Most general anestheticsshouldn't be like that.
But you're gonna the mostunstable critical patient you've
ever had at bedside, you'll haveso much more in the operating
room.
You'll have so much moreresponsibility.
So really solidifying yourfoundation, learning as much as
you can about these drugs, andgetting that really good
experience, taking care of thosesuper sick patients, is going to
(33:24):
help prepare you for thattransition and that role into
being an anesthesia provider.
All right.
I've really enjoyed this.
Uh got to ask a bunch of peoplehave to ask a bunch of good
questions.
Uh don't forget to check out ourwebsite at CRNA School Crep
Academy.com.
Come to our Louisvilleconference in June, and uh
remember to check out uh ourlink tree.
(33:47):
We've got a great uh communityon Circle.
And by all means, you know, ifif you're not a member yet,
consider joining.
We have info sessions uh acouple times a week, and you'll
get a lot of valuable, uhvaluable resources as you're
looking to apply and go to CRNASchool.
Awesome.
Thank you all very much.
(34:07):
Have a wonderful rest of yourday.
Jenny Finnell (34:10):
Thank you for joining us on the Sierra Nation
School Prep Academy podcast.
We hope today's episode gave youclarity and confidence for the
road ahead.
Keep showing up for your goals,keep learning, and keep
believing what's possible foryou.
We're always rooting for you inyour future as a CRNA.
Until next time, take care.
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