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Pressors and Vasoactives

Hi all heres a new update of our first-ever article. As usual, please remember that these articles
do not mean to be the final opinion on anything! They are only meant to reflect our own
experience and knowledge, which is scary getting up to about 50 years combined. Always
check with your own references and authorities! And when you find mistakes, let us know?

What is a pressor?
What is shock?
Are there different kinds of shock?
What are the three parts of a blood pressure?
What does pump mean?
What is inotropy?
What about volume?
Whats crystalloid?
What is squeeze?
How does this relate to shock?
10-1- PA Lines
10-2- Something that will make you look really smart!


Which shock state reflects a pump problem?

What is ejection fraction?
Which shock state reflects volume?
Which shock state reflects arterial squeeze?
What measurements do we use at the bedside for treating shock states?
How do pressors fit into the treatment of shock states?
How do pressors work on receptors?
17.1Agonizing receptors
17.2Antagonizing receptors


How are other shock states treated?

Are pressors used to treat hypovolemic shock? An important point. Another one.
What about cardiogenic shock?
What other pressors are there?
What basic considerations should I keep in mind when using these drugs?
22-1- Setting up the drips.
22-2- Drug rates.


Are there other vasoactives that I need to know about?

How do we use vasopressin?
Why dont we use the Trendelenburg position for hypotension anymore?
A Chart Thing for those who like them

The Quiz!

1- What is a pressor?

Blood pressure medicines come in a couple of varieties: there are some that make blood
pressure go up, and there are those that make it go down. The word pressor is usually used to
mean the first kind. Another word that describes these drugs (both kinds) is vasoactives, which
is to say: affecting blood pressure, or heart rate, or both. The major use for pressors is in the
treatment of one kind of shock or another.
2- What is shock?
n. (noun)
1. Something that jars the mind or emotions as if
with a violent unexpected blow.

2. The realization that you are working in the MICU

Shock is usually described as a state in which the bodys tissues arent getting enough blood flow
for one reason or another. The peripheral tissues way away from the major vessels, and
supplied by smaller vessels whose perfusion suffers when blood pressure drops lose much of
the blood supply that they depend on for oxygen and nutrient delivery. So they switch gears at the
cellular level: they change from aerobic respiration, in which they use delivered oxygen to make
energy, to anaerobic respiration, which works, but poorly. The byproduct, or engine emission of
aerobic respiration is carbon dioxide, which we get rid of by breathing. But the emission from
anaerobic respiration is unfortunately lactic acid, and since the blood vessels are not carrying
wastes away effectively being underperfused the lactic acid builds up, creating a metabolic
acidosis. The acidosis makes blood pressure even harder to maintain, since most pressors like
adrenaline (epinephrine) and norepinephrine (levophed) depend on the blood pH if the pH is too
low, they wont work very well.
3- Are there different kinds of shock?
Yes three main ones, but to understand them, we need to talk about how exactly a blood
pressure is maintained. It turns out that there are three major components of a blood pressure.
4- What are the three components of a blood pressure?
We think of them as: pump, volume, and squeeze. Of course, its lots more complicated
than that, and as always, most of the information in all of these articles is written with a lot of lies
thrown in there are shelves of textbooks that have been written on each subject that we try to
cover in a few pages. But the point is: how can you organize the ideas in your head to figure
things out at the bedside? Quick-and-dirty is what will help most
Keep in mind as we go along that each of these components needs to be measured, and that
many of the tools we use in the unit are designed to do just that.

5- What is pump?

Pump is the heart. Anything interfering with inotropy, heart rate,

or cardiac output, be it an MI, an arrhythmia, ischemia is a
pump problem.
How might you measure your patients ability to pump?
Numerically, I mean?

6- What is inotropy?
Inotropy means: how hard the left ventricle is working to pump, to empty itself.

Thats this one. Why do we worry about the left

ventricle so
much, in relation to blood pressure? I
mean, we worry about
the RV too but for sort of
different reasons. Take a look at
the article on PEs for
more about this.
Hmm think we could measure this?

7- What about volume?

Easy enough: the circulating volume in the blood vessels. You have to
include the relative volumes of red cells and plasma to this idea
though there may be plenty of red cells, but if a patients plasma
volume is low which is to say shes dehydrated, hypovolemic, but
not from bleeding you wouldnt give that person blood, would you?
Or the other way around you wouldnt give just crystalloid to a
person with a low crit from bleeding, would you?

8- No. Whats crystalloid?

Any clear-as-crystal IV fluid is crystalloid its a word used for a kind of

IV volume replacement - as opposed to colloid, meaning anything proteinbased such as albumin of one kind or another, or plasma but as I
understand it, not red cells. Anyhow, right you would correct volume loss
with what the person needed, based on what they needed: red cells, or the
water component of the circulating volume.
How might you measure your patients volume status?

9- What is squeeze?
Squeeze has actually been used around ICUs for long time
to mean two different things some people use it to describe
how tight the arterial bed is - which is to say how tight, or
constricted the entire system of arterial vessels is. Other
people use squeeze to mean inotropy. I use it the first way,
because it helps me think about whats happening to the
patient its a useful concept when youre faced with a
hypotensive situation that youre trying to sort out.
We need to measure this too

10- How does this relate to shock?

The three components of a blood pressure actually reflect the three kinds of shock that youre
likely to see in intensive care. The trick in treating each of these correctly comes from our ability
to measure each of the components precisely. Any idea how we might do that?
10-1- The tool you need in this situation is a PA line a pulmonary artery catheter, also knows as
a Swan-Ganz line, or just a Swan.

Thats the yellow thing, going into the blue thing,

there at the patients ear, sort of? Which is
connected to the white thing, going into his

PA lines tell you everything you want to know:


how well the pump is pumping (cardiac output, cardiac index)

how full the right side of the heart is (CVP), and how full the left side is (wedge
pressure) thats the volume

and how well your patients arteries can squeeze : thats the SVR the systemic
vascular resistance

PA lines are serious juju theyre invasive, theyre tricky to place, they need very serious care
and feeding in fact, theyve got a whole enormous FAQ all to themselves, and they need one!
But understanding how pump, volume and squeeze all go together is important to understanding
how pressors work. Go take a look! (
10-2- Something that will make you look really smart.
An alternative if your patient has no PA, but does have a central line and a radial a-line, you can
call the in-house IABP tech to come and do a green dye cardiac output. They hook up a little
color-measuring thing to the arterial line, and they inject some form of dye - (probably green!) through the distal port of the CVP. Then they measure how long it takes for the dye to show up at
the a-line, multiplied by this, divided by that, aligned with the coefficient of Hammerschmidt, over
the square of the patients shoe size and out come the numbers. Cool!
11- Which shock state reflects a pump problem?
The kind of shock that reflects pump failure is cardiogenic shock, which is to say: originating
in the heart. Simple idea: the blood pressure is low because the pump isnt pumping. This is
usually because of a sizable MI, but people with end-stage heart disease of one kind or another,
such as cardiomyopathy (heart-muscle-disease), or people who have had multiple MIs - leaving
them with a very low ejection fraction - can live on the edge of cardiogenic shock much of the
12- What is ejection fraction?
EF is the amount of blood ejected from the
left ventricle into the arterial circulation with
every systolic contraction, expressed as per
cent. Normal is something like 50-70%.
Impressively low is usually said to be less than
30%, and cardiac cripples who cant get up
from the chair without shortness of breath
sometimes run in the low teens.
Heres the LV at the end of diastole all full,
ready to go.

Heres the LV at the end of systole the

LV is contracted. 45% of the blood in the
LV is left, so 55% has been ejected into
the aorta.
See? Thats pump. So what happens
if the pump cant pump?

13- Which shock state reflects volume?

Hypovolemic shock reflects low volume and again, the fix depends on which component of
circulating volume the patient has lost. You probably wouldnt give red cells to a patient with heat
stroke, whose crit might be up around 60%. And you would try not to give crystalloid to a person
with a big blood loss. Would you give this patient a pressor?
14- Which shock state reflects arterial squeeze?
Septic shock reflects squeeze. (Cardiogenic shock affects squeeze too, but we get into that
in the FAQ articles on PA lines and balloon pumping ( take a look at
those for more than you ever wanted to know on the subject! )
It turns out that the arteries are contractile they can be made
to open up (dilate), or tighten up (constrict). The whole
system of arterial vessels is sometimes called the arterial bed
and it helps to think of the whole bed, the whole system,
loosening or tightening up in response to various states.
In septic shock, the germs floating about in the systemic
circulation produce a set of unpleasant chemicals called
endotoxins. These specifically affect the arterial vessels - they
loosen up, causing the blood pressure to drop. An analogy
would be a garden hose turned on full if you squeeze the
hose, the pressure rises, and the water squirts across the yard.
If you release the squeeze, the water pressure drops, and the
water runs all over your shoes. Similarly, if the arterial system
as a whole tightens up, the patients blood pressure rises, and if
the system loosens up, the pressure falls which is the cause of hypotension in septic shock.

So the trick in diagnosing hypotension is to figure out: which of the three components is the
problem? Theres lots more on this subject in the PA-line FAQ.

15- What measurements do we use at the bedside in the ICU for treating shock states?
Well, we start with blood pressure, but you probably knew that part. Use the tools at hand. A
blood pressure cuff is a good start. A seriously hypotensive patient, on pressor drips, really ought
to have an arterial line.
The same catheter as an IV, usually
a 20 gauge angiocath, inch and a
quarter, in the radial artery, hooked
up to a transducer.

A labile blood pressure an unstable one needs constant monitoring, because well,
because its unstable! The need for pressor titration (dialling the dose up or down) is ongoing
you want to wean these drips down whenever you can, while still keeping the blood pressure in
the range your patient needs. An actively septic patient, or a cardiogenic one, can require pressor
titration every few minutes! You didnt think you were going to get to sit down in the ICU, did you?
(grin!) If you dont have an a-line use the non-invasive BP cuff, and set it to cycle frequently.
How frequently? What if the patient is coagulopathic? What is coagulopathic? What if she has a
low platelet count? What is a low platelet count?
Then there are the central line numbers: CVP, wedge pressure, and the ones we get from
shooting numbers: cardiac output/ index (CO/CI), stroke volume (SV), and systemic vascular
resistance (SVR). Each of these measurements corresponds to one or the other of the three parts
of the blood pressure, and each kind of shock has a characteristic appearance that is often
immediately obvious one you shoot your first set of numbers after a PA line goes in.
16- How do pressors fit into the treatment of shock states?
The choice of pressor depends on the nature of the problem. To explain this, a quick review of
adrenergic receptors will help. There are three adrenergic receptor sets that we worry about in
the ICU: the alpha receptors which are located in the arteries, and the two kinds of beta
receptors: beta-1s (you have one heart, thats where they are), and beta-2s, (you have two
lungs, thats where those are.)
17- How do pressors work on receptors?
This is really helpful to understand:
17-1- To agonize set of receptors means to stimulate them, to make them do their thing. If you
agonize the alpha receptors in the arteries (a little repetition never hurts), then the arteries
tighten up.
17-2- To block, or antagonize those receptors means to stop them from doing their thing.

If you antagonize the alphas, then the arteries loosen up. (This is how some antihypertensives
work: doxazosin/ Cardura, terazosin/ Hytrin, prazosin/ Minipress. Hydralazine too, maybe?)
17-3- You might remember that the number we use to measure how tight or loose the arterial
system is as a whole is the SVR the systemic vascular resistance - the normal range is
something like 800-1100. The thing to remember is: higher is tighter, lower is looser. So to take
the example of sepsis, the basic problem producing the hypotensive, acidotic state is that the
arterial system has been made to dilate by the action of bacterial poisons floating about in the
bloodstream. Low SVR. To counter that dilation, we use (usually) a pure alpha-agonist pressor:
neosynephrine (phenylephrine). Neo agonizes the alphas, and makes the arteries tighten up
again. So the SVR, which might be as low as 200-300, should rise as the arteries constrict. In
sepsis, the pump isnt the problem, its the squeeze thats not right.
The volume component becomes a problem too in sepsis, since as the arteries dilate, the volume
in them is suddenly not enough to keep them filled up so the CVP and wedge pressure are low.
People describe this by saying the tank is dry the tank being the capacity of the arterial
system, which has just been increased dramatically by dilation. The heart tries to compensate for
the loss of arterial squeeze and volume by pumping both harder and faster, so the classic
appearance of the numbers is: high cardiac output and index, low SVR, and high heart rate.
The strategy against sepsis is simple:

fill the tank: hydrate the patient to increase her circulating volume,

squeeze the tank: apply an alpha pressor to tighten up her arteries.

kill the bugs: find the source, and give her the appropriate antibiotics.

Nowadays theres been a big move to act more aggressively when sepsis rears its ugly head,
and there are a number of rules for treating it in the early stages, based on a whole lot of review
work done by some eminent docs led by R. Phillip Dellinger. In my ICU, these translate into a set
of specific steps that elaborate on the three rules I made up myself (grin!), and involve rapid
hydration something like 8-10 liters over the first six hours (whoa!); measurement of CVP and
central venous oxygen saturation with specs drawn from the distal catheter port, careful
application of pressors to achieve MAP goals and preserve organ perfusion, tight control of blood
sugar levels stuff like that. Good stuff!
Levophed is often used interchangeably with neo, but has broader effects on both sets of
receptors, which sometimes produces problems: for example, a patient in sepsis will already be
reflexively tachycardic. Sometimes levo can aggravate the tachycardia , sometimes disastrously,
producing unpleasant things like rapid AF, or even nasty ventricular arrhythmias think of using
neo in this situation.
18- How do you treat other shock states?
The other two states that we see are hypovolemic and cardiogenic shock. Hypovolemia is treated
by fluid resuscitation with the appropriate component of volume that the patient needs: red cells
(along with stopping the blood loss), or crystalloid for dehydration. In hypovolemia, you see a
similar picture to sepsis in that the heart rate rises to compensate for loss of circulating volume,
and the central pressures: CVP and wedge will be low, but the SVR will actually rise very high
maybe up towards 2000, because the arteries will tighten up to try to maintain blood pressure.
These folks make lactic acid out in the peripheral tissues not because their arteries are too loose,
but because theyre too tight, and the little arterioles cant get their supply theyre shut out of the
circulation, out there at the toes and fingers and the like. These people have cold, sometimes
dusky hands and feet.

19- Do you use pressors to treat hypovolemic shock?

Not if you can avoid it. If blood pressure doesnt recover with the right kind of fluid treatment, then
something else is probably going on. If you apply an alpha-agonist pressor to an empty tank,
youll tighten the arterial system to the point where the patient may lose their fingers or toes to
necrosis. If you apply a beta-agonist pressor to increase the heart rate well, their heart rate is
already up, isnt it? A patient with this kind of reflex tachycardia can be pushed from sinus tach
into something like rapid AF or even VT by using a beta agonist pressor this is why levophed
sometimes doesnt work in septic situations the way you want it to. Lately theres been a move to
dobutamine (pure beta agonist) in septic situations, and while it may make scientific sense, it
seems like a dicey move to me, for the same reasons, so be careful.
Dopamine has similar effects its chronotropic that is, it raises heart rate, even at low doses,
and because its often the only pressor available for peripheral use, it is used in situations where
it probably shouldnt be although in a code, or near-code, you do what you have to do to save a
life. If theres no option but to run a vasoconstrictive pressor through a peripheral vein while the
team is getting, say, a femoral line placed well, thats what you have to do. Change over quickly
the patient could lose an arm if the drug infiltrates!
An important point:

Regitine/ phentolamine. This is worth knowing about if your patient manages to

develop an infiltration of a pressor, probably through a peripheral vein, whats going
to happen to the tissues at the site? Why?
Regitine is the drug for this situation: its an alpha-blocker. What the docs will do is
draw it up in a syringe, and with a subcutaneous injection needle, theyll infiltrate this
stuff into the tissues around the IV site, hopefully reversing the alpha effect of the
pressor. Apparently it works Ive only seen it done once or twice, but you might
save someones arm this way

Another important point, and a specific caution about central lines should go here. A central line
placed emergently for giving pressors is a good thing its the right thing to do but you need to
make sure that its in the right place. Youre using the line, its your responsibility. Once the patient
gets to you, wherever that line is: transduce it. Youll immediately get lots of arguments about
whether or not the number is real, and all this, but thats not the point. Youre trying to make sure
that youre not sending pressors downstream, towards the leg, right? What would happen in that
case? What if the line wasnt in a vessel at all maybe in the peritoneal cavity? What then?
So transduce the line. If its arterial youll know! If its venous, youll know that too. Who cares
if the number is correct as long as theres a CVP waveform of some kind, and the mean
pressure is about, say, 12, and not 60 youre probably ok. So what does a CVP waveform
look like?
Another update: phenylephrine (neo) can now be given peripherally in a dilute mix of 10mg in
250cc, but should only be used temporarily while the patient is waiting to have a central line
inserted. Try to use a big vein. We got a patient last week with a peripheral mix of levophed
running: 4mg/ 250cc bag I dunno about that one. They tried to tell me it was policy I have to
ask about that. Sounds hazardous.

20- What about cardiogenic shock?

Cardiogenic shock is produced by pump failure usually from a big MI. In this case, the set of
adrenergic receptors to work on are the beta-1s, and the pressor to apply in this situation is
dobutamine a pure beta pressor. (Assuming you want to use a pressor at all. You dont want
to whip an already failing left ventricle if you dont need to you use an intra-aortic balloon
pump another FAQ.)
You have 1 heart thats where the beta-1s are. The numbers for cardiac output, central
pressures and the SVR form a pattern that is just as classic and recognizable to the
experienced ICU person as the ones for sepsis: in this case, cardiac output is low (because the
problem is with the pump), and the wedge pressure will probably be high, since the left ventricle
cant empty itself, and the pressure backs up.
(If the pressure continues to back up, the rising pressures will reflect back to the lungs, forcing
water out of the capillaries into the alveolar spaces congestive heart failure this is why
cardiogenic patients are almost always intubated.)
The SVR will be high - as in hypovolemia, the only reflex the body has available to try to keep up
the blood pressure is by tightening the arterial bed. (Youll notice that this is the mirror reflex of
the one the body uses in sepsis tachycardia/ increased inotropy. There are only the two reflexes
the body has available to use in these situations. Well thats a big lie. But you get the idea )
Agonizing the beta-1s increases both heart rate and inotropy, which increases cardiac output and,
hopefully, blood pressure. Be careful! Beta-1s can often be stimulated by beta -agonist drugs
used for other reasons: the classic one is albuterol supposedly only a beta-2 agonist. Beta-2
receptors are in the lungs (you have two lungs): when you agonize them, the bronchi dilate. But
these drugs arent all that specific: albuterol can kick the heart rate up as well as opening up
bronchi. Increased heart rate in cardiogenic shock = badness.
The opposite case is also true: giving a beta antagonist, or beta -blocker, like Inderal, can have
a bad effect on the beta receptors in the lungs producing broncho-constriction (asthma attack!).
Lopressor is supposedly beta-1 specific, and hopefully leaves the lungs alone. Just something
to think about. Might want to switch to verapamil.
21- What other pressors are there?
We talked a little about dopamine above. Dopamine effects come in three flavors, related to the
dosage being given: low, medium, and high. At low doses, say 150-300 mcg/minute, dopamine is
thought to affect dopaminergic receptors, which in turn is supposed to increase blood supply to
the kidneys : this is what they mean by renal-dose-dopa. Does it work? People argue about this
one all time in very learned fashion, but it seems to work enough of the time that we still do it
At middle ranges: 300-600 mcg/minute dopamine has beta effects it increases heart rate and
inotropy. Theres lots of overlap in these ranges, and many is the patient started on renal dose
dopamine whose heart rate pops up to 150 time to shut it off! Again, this is probably not the
pressor to use in a septic situation, because the heart rate is already too high, right? So applying
a beta-agonist pressor may push the septic patient with sinus tach at 150, into rapid a-fib at 200,
or even VT. At high ranges: 600-1000 mcg/ minute using the ancient method of the straight-drip
technique (as opposed to the mcg/ kg/ minute technique that everybody else in the universe
uses), dopamine finally has some alpha effect. But do you want to push a tachycardic patient all
the way through the beta range, to finally get to the alpha range to get their blood pressure up?
Negative! Use neo.

Another couple of pressors, more rarely used: epinephrine, which is a kitchen-sink, kickeverything pressor, hardly used except in codes and as a last-ditch in hypotension thats not
responding to anything; isoproterenol (Isuprel, or just Prel) a very powerful beta-agonist,
really rarely used, only as a bridge to try to keep heart rate up in situations where atropine doesnt
work the drill used to be: A-I-P for symptomatic bradycardia: atropine, isuprel, pacing wire.
Nowadays we use the Zoll pads.
22- What basic considerations do I need to keep in mind about using these drugs?
A few words about using vasoactives in general: try to think about how the drug is being delivered
to the patient: is anything (besides you) speeding up or slowing down the flow? Sometimes big
changes in blood pressures can mean that somebody gave, say, an antibiotic through a line
carrying levophed. Big mistake. This would initially cause a dramatic rise in BP, followed by
many inches of IV tubing carrying no pressor at all (and if the flush is running at 5cchr, it may take
two hours for the pressor to fill the line back to the patient!)
22-1- Setting up the drips:
Precise, consistent delivery is your goal. Heres what to do:
Hang a bag of normal saline, with tubing, on an infusion pump, (not a gravity line!), set at a
fixed rate. This is your flush line. Choose a rate that is going to deliver the vasoactive fairly
quickly not 10cc/ hour! You can turn it down later, but if your patients blood pressure is squat,
you want to deliver the pressor fairly quickly. This does not meaning bolusing the patient with
pressor it means getting the column of the drug delivered to the patient quickly.
Now the question is where to plug the pressor into the flush.
Not coming up with the
best pictures, but you
can see the basics
Heres the part that
spikes the bag
and heres the end of
the line, closest to the
and heres a y-site
connector, where you
plug things in

So the question is where do you want to plug in your pressor? And why does it matter?
Well the whole point is that you want your patient to see this drug pretty soon! If youre using
the little syringe pressor mixes, they run at rates of what a cc? Per hour? Vasopressin runs at
2.4 cc per hour. If your flush line is running at 10cc/ hour, and the tube holds, say 30cc, and you

plug the vasopressin into a y-connector halfway up the line it might be hours before the patient
sees the drug!
You dont want to hook up the syringe directly to the infusion port either a drip running at 2.4 cc/
hour isnt enough to keep the lumen from clotting off thats what the flush is for.
So okay you dont want to use the y-connector what to do?
Grab one of these a stopcock manifold. Stopcocks are
something you may not see until you get to the unit, and they
take a little getting used to, but theyre essential. Very useful.
Heres just one
And heres a bunch of them connected together a

Screw the manifold onto the end of the flush line tubing, and the other end onto the infusion port
of the patients central line. Now screw the luer connector of the pressor into one of the manifold
connections. This is easier to do than it is to describe
Now your pressor is connected as close as possible to the patient, and being driven by the flush
line. This means your patient will see the drug soon.
I try to use flush lines running at a fixed 100cc/ hr when possible this means that the pressor is
never going to take very long to reach the patient down the line. Whenever possible, run
(compatible!) vasoactives at constant rates, and with a line all to themselves. Try not to change
the rate of a flush attached to a pressor line rapidly move in small increments, and try to be
Never (really never!) bolus patients with pressor during hypotensive episodes. These are
the big gorillas of the drug world, and you can kill your patient with them! Make sure the drug is
actually reaching the patient at a controlled rate, and make small changes. Be patient! Anticipate
big changes when increasing pressor rates, and be ready to dial down rapidly when you first see
the change youre looking for.
Also dont get into the habit of turning the flush rate way up briefly if your patient goes
hypotensive. Turn it up a little! It can be very hard to be patient, with the team breathing down
your neck remember that if you do give a bit of fluid through that line, that youve washed all
the pressor out of it, and youre going to have to wait all over again for it to work, which means
the patient will get hypotensive again
22-2- Drug Rates:
Lets talk briefly about rates. In almost every hospital in the universe, vasoactive drugs are
delivered based on the patients weight, measured in kilos, over time. So the dosage is measured
in micrograms per kilo, per minute. This standardizes the dosage number from one patient to the
next, no matter how big or small they are, which makes thinking about it relatively easy. An

example is dopamine: low medium and high range effects are supposed to roughly correlate with
sections of the range, from 1 to 10 mcg/ kg/ minute. Maybe up to 12.
We do it a bit differently we run straight drips, which just means setting the pump to deliver,
say, 200 mikes of dopamine/ minute. Its easy, and in practice, youre titrating the drug for effect,
right? So it doesnt really matter what dose technique you use, as long as you stay in the
ranges in your policies. Check them frequently!
Heres a quick example of how it doesnt matter: lady came in, bad heart, low EF, PA line, the
docs want to try one drug, then another, to see if they can tweak her cardiac output. Actually, she
was lying there in the bed on 2 liters of oxygen, quite comfy, good blood pressure, mentating, but
shed recently developed acute renal failure, and the docs are all a twitter to technologize her and
optimize her, and this, and that the older nurses are looking at each other: She looks fine! Why
dont they just leave her alone?
So anyhow, they float in a PA line. Poor lady. Now we start shooting numbers, and they ask me to
start dobutamine I think they were hoping for a little inotropy, a little afterload effect if possible, a
little this, a little that so the intern calculates her weight, which is pretty impressive, and then
calculates the straight drip rate, and turns to me, and says: Ok, so go ahead and start her on 300
mikes per minute.
No way, man. I am an old, beat-up, battle-weary ICU nurse, and Ive seen many and many a bad
thing happen over the years even low doses of dobutamine can produce an impressive
tachycardia not a good thing for a hurting heart. So I mention this in a friendly way, and, what
with the grey hair and all, I convince him that Im going to start at 100mcg instead. He has this
look: Ok, Ill indulge the old nurse. Poor old guy.
An hour later, the ladys heart rate has gone from 74 to 118. Shes not getting sweaty or having
chest pain yet I go and grab intern boy. We change to a different drug.
See the point? Sure, she was way below the calculated dose range expected for her size. But:
responses to these drugs are extremely variable. She hadnt read the interns textbook.
23- Are there other vasoactives I need to know about?
We havent talked much about the other kind of vasoactives: the ones that make blood pressure
go down instead of up. These come in a couple of flavors:

Receptor antagonists: The opposite of an adrenergic pressor. I dont think theres a

pure alpha antagonist blocker drip that I can think of, although remember regitine?
The alpha blocker? Only used for infiltrations
You will see labetolol this is a cool idea: its both an alpha and a beta blocker so
it loosens a tight arterial bed when your patient is hypertensive, and slows his heart
rate as well. Nice!
Otherwise, youll see beta-blocker drips sometimes for heart rate control: propranolol
sometimes, sometimes esmolol stinky drug, works poorly. (Did I really say that?),
and sometimes calcium-channel blocker drips: diltiazem mostly I think. Works much
better than esmolol, as far as I can tell.

A drug sort of in a class of its own which does about fourteen nice things at once for
the heart is Amiodarone. Neat drug it has complex effects, including beta
blockade, and the ability to sometimes chemically convert people out of a-fib. Or vfib! Very cool!

Nitroglycerine (TNG) is used for controlling anginal symptoms and for acute blood
pressure control (it doesnt seem to work very effectively for this in most people) it
works by dilating both arteries and veins, decreasing SVR (afterload) and preload, by
increasing the venous capacity. Less volume arrives at the LV because the venous
tank is bigger, and its easier to pump it out, because the arterial tank is bigger looser.

Nipride (nitroprusside) is the third antihypertensive that we use. This is the Big
Gorilla in the antihypertensive zoo. Be extremely cautious with this drug it is
very powerful. (Some people call a nipride bag wrapped in foil the silver bullet.) It
must always have a separate, dedicated IV lumen all to itself, and nothing must
ever be run through that line it will bottom out your patients pressure.
The bad thing about nipride is that it works so rapidly you have to move very
carefully when titrating up on the dose.
The good thing though about nipride is also that it works so rapidly it has a very
short half-life, and within seconds after you stop the infusion, its effects (should!) go
away. Nipride can produce a really poisonous cyanide metabolite called thiocyanate
usually this gets measured at least daily while a patient is on this drug. Worse in
renal failure.

24- How do we use vasopressin?

Vasopressin, which is also ADH? Anti-diuretic hormone?, is used in several situations in the
MICU, but mostly, lately, for sepsis. The confusing thing is that the ranges are very different.

For GI bleeding, the range is 0.1 to 0.4 units/minute. Nowadays weve mostly gone to
octreotide for this situation, but its worth mentioning.

For use as a pressor in sepsis, the dose is 0.04 units/ minute. Sometimes we wean it
to 0.02, but mostly we just shut it off when the patients pressure recovers.

The theory as I understand it (not very well), is that in sepsis the body gets into a vasopressindeficient state, which contributes to the systemic arterial vasodilation. I have to say that Ive really
been surprised at how effective this stuff is actually the really impressive part for me was how
SVR recovers with this drug. Its a weird but true fact that applying regular pressors to a septic
patient with a PA line well, the BP comes up, for sure, but the SVR often stays low really low,
in the 300s, maybe. I have no clue why youd think it would rise as the pressure did. Not until
vasopressin came along did the numbers actually start to reflect what youd expect.
The other significant thing about vasopressin is that youll see your patients heart rate drop,
sometimes down from say, the 130s, to around 60 or 70. It may take a day or longer for the heartrate effect to show up, but blood pressure usually responds within an hour or so in my
experience. This can make your team nervous weve seen some patients on vasopressing get
into bradycardias in the 40s, with serial EKGs, troponins, much head-scratching remind the
team that it may be the drip. Theyll look at you as though youre mad, until the attending comes
in and agrees with you. Then theyll look at you as though youre magic, which is just as bad

Vasopressin has also showed up in code situations, which was new to me at the last code I
went to, I found myself pushing a vasopressin dose, which made me a little nervous
We also give a drug called DDAVP/ desmopressin, which is a synthetic version of ADH,
sometimes for uremic bleeding, and sometimes rarely for people who dont make their own
ADH. Diabetes Insipidus. Remember that diabetes means siphon water goes in, and
comes out almost at the same speed! We had a young man a year ago who was pan-hypopituitary, after a brain tumor was removed. Didnt make any ADH. So if he missed his DDAVP pill
(used to be nasal spray, now I guess theres a pill), it was like Niagara Falls in his room until we
could get it into him! So its good to know that theres an endocrine aspect to hemodynamic
management too, although you dont see it too often
25- Why dont we use the Trendelenburg position for hypotension any more?

Ok which one is this?

And this?

This one was hard for an old nurse to get used to after doing it for something like 20 years,
another piece of basic knowledge gets chucked out they say that putting patient in T-berg
makes blood flow north in the patient, increasing the intravascular pressure on the carotid bodies,
making them think that things are better than they are. Remember that these are the guys who
live in the aortic arch, looking downwards toward the heart. If the amount of volume coming out of
the LV suddenly drops, they get on the line to the adrenals saying: Yo! Secrete some epi! So if
you put the patient in Trendelenburg, they see this as more volume (which it isnt, really), and it
just defeats your whole purpose. Plus it makes it hard for the patient to breathe. Jayne says that
the best thing to do is to: Lie em flat, and put their feet up on two pillows, which will improve the
blood pressure some because it improves the venous return. Sounds good to me. But I have yet
to see a patient lose blood pressure in T-berg
What I have seen is reflex bradycardia when patients are inadvertently bolused with some
powerful pressor. Typically someone gets impatient with waiting for a pressor change to take
effect, and dials up too rapidly. The patient will suddenly respond with a blood pressure that may
rise from, say, 70 up to 240 systolic this does indeed produce a reflexive bradycardia, which is
the carotid bodies doing the other thing, yelling Whoa! down the phone line.
Dont give this patient atropine! Just dial them right back down again, or even shut off the
pressor/flush flow altogether for a short time, then carefully re-titrate. You have to be a little
patient with pressor changes be alert to this situation in the ICU. A patient with a sudden drop in
heart rate, and a sudden spike in blood pressure on the bedpan? Or did someone get hasty
with the Levophed?

26- Heres a little Chart Thing for those who like them:
Condition CVP/PCW CO/ CI SVR SV Pressor to Use? Receptor to Treat

8-10/ 10-12 4-6/ 2-3 1000 80+/



Neo, Levo, Vaso Alphas

Cardiogenic: +/-



Fluid or blood only?


Beta-1s IABP?

The Quiz!:
Ready for the quiz? No answer key! Any and all of the answer choices may be relevant! Discuss,
compare and contrast!
1- Pressors are:

drugs that press on things

pills that raise blood pressure
pills that lower blood pressure
very precisely titrated intravenous drips, which work on specifically targeted
adrenergic receptors, and which are carefully chosen depending on the situation
of the patient
e- I give up!
2- Vasoactives are:
a- drugs that act on vaso things
b- different kinds of Vaso-line
c- the name for pretty much any kind of drug infusion that affects heart rate,
peripheral arterial or venous constriction, dilatation, and therefore blood
pressure, along with the size of the pupils
d- I lied about the pupils
3- Shock is:

how you feel when you come to work in the MICU

when your patient has low blood pressure
when she has high blood pressure?
Low blood pressure, for any of three main reasons, causing peripheral lactic
acidosis, and a lawnmower
e- B and d, except for the lawnmower
4- The three parts of a blood pressure are:
a- pump, crackle, and pop

b- snap, squeeze, and Dopey

c- squeeze, pump, and volume
d- Huey, Looey, and Sneezey
5- Cardiogenic shock results from:

pulmonary failure
a big MI
a low EF
a high EF?
B and C

6- Volume is measured with:


a CVP line
an arterial line
a foley catheter
a blood pressure cuff
feeling the inside of your patients mouth for moisture

7- Pressors are for:


all shock states

some shock states
Only states where theyre allowed by law
Certain shock states, depending on what the cause is

8- How many adrenergic receptors do we think about?



9- Pump is measured, numerically, using:


cardiac output
cardiac index
pulmonary output
pulmonary index

10- Squeeze is measured with:


a girdle
a PA line
a green dye output

11- To agonize a receptor means:

a- To really hurt!
b- Just to make it a bit nervous
c- To generally increase the tone and activity of the organ that its attached to

12- To antagonize a receptor is to:

a- make it angry
b- to generally decrease the activity of the organ its attached to
13- The pure alpha pressor that we use is:


14- The pure beta pressor that we use is:



15- Vasopressin is:


run at a rate of 0.4 units per minute

run at a rate of 0.04 units per minute
run at a rate of 4.04 units per minute
run at a rate of 44 units per minute

16- An infiltrated peripheral pressor:

a- is no big deal, nothing to worry about
b- might be a big deal, but nothing to worry about
c- an incredibly big deal, that you really have to worry about, that you should
do your utmost to prevent, that could cause the loss of the patients limb,
and which should be immediately reported to the physicians, assessed,
and possibly treated with a regitine infiltration
d- whats an infiltration?
True or False:
17- All central lines should be transduced as soon as possible, to make sure theyre in the
right vessel.
18- All central lines should be transduced as soon as possible, to make sure theyre in the left
19- I can run my pressor drips through a gravity flush line.
20- I can run bag mixes of pressors on a gravity line.
21- I can run Nipride on a gravity line. (Shudder)