Download Pressors and Vasoactives

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Pressors and Vasoactives
Here’s an update of the 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? Thanks!
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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”?
What’s “crystalloid”?
What is “squeeze”?
How does this relate to shock?
10-1- PA Lines
10-2- Something that will make you look really smart!
(Or really antiquated :))
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?
17-1 - Agonizing receptors
17-2 - Antagonizing receptors
17-3 - SVR
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 don’t we use the Trendelenburg position for hypotension anymore?
A Chart Thing for those who like them…
The Quiz!
A note on updates: “the only constant...
is change”.
Wow, is this ever true. It often seems
now that every time we do something,
check a procedure, or look up a topic –
it’s different. Lots and lots of things are
coming under the increasingly powerful
scrutiny of “evidence-based practice” –
this is only a good thing, and surely
makes perfect sense. It’s very
interesting when bits of “received
wisdom” turn out not to be true... we
just got rid of TEDS! Heresy!
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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.”
http://www.thefreedictionary.com/shock
2.
The realization that you are working in the MICU…
http://media.photobucket.com/image/shocked%20face/unclewulf/hayden_shocked_face_resized.jpg?o=11
Shock is usually described as a state in which the body’s tissues aren’t 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 won’t 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, it’s 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? Quickand-dirty is often what will help most…
Keep in mind as we go along that each of these components can be measured, and that many of the tools
we use in the unit are designed to do just that.
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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 patient’s ability to pump? Numerically, I
mean?
http://www.klangundkleid.ch/img/moebel/sofina/08510_double-stroke-hand-pump.jpg
6- What is “inotropy”?
Inotropy means: “how hard the left ventricle is working to pump, to empty itself”.
That’s this one. Why do we worry about the left ventricle so
much, in relation to blood pressure? Actually, we worry about
the right ventricle too – but for sort of different reasons. Take a
look at the article on PE’s for more about this.
(www.icufaqs.org/PulmonaryEmbolism.doc)
Hmm – think we could measure this “LV inotropy”?
http://www.everyschool.org/u/wcms/tanaka/Heart.jpg
7- What about “volume”?
Easy enough: this is 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 patient’s plasma volume is low –
which is to say she’s dehydrated, hypovolemic, but not from bleeding – you
wouldn’t give that person blood, would you? Or the other way around – you
wouldn’t give just crystalloid to a person with a low crit from bleeding,
would you?
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8- No. What’s crystalloid?
Any “clear-as-crystal” IV fluid is “crystalloid” – it’s a word used for a kind of IV
volume replacement - as opposed to “colloid”, meaning anything protein-based
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 patient’s volume status?
http://www.fluvaccine.com/Stat/images/itemslarge/2U4.jpg
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 to
think visually about what’s happening to the patient – it’s a useful
concept when you’re faced with a hypotensive situation that
you’re trying to sort out.
We need to measure this too…
http://www.mikkis.co.uk/admin/images/Stressball-Home.jpg
10- How does this relate to shock?
The three components of a blood pressure actually reflect the three kinds of shock that you’re 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 known as a SwanGanz line, or just a “Swan”.
That’s the long yellow thing, wrapped in the clear
plastic thing, going into the blue thing, there at the
patient’s ear, sort of? Which is connected to the
white thing, going into his neck?
In proper terms: the PA line, inside its clear sheath, is
advanced into the patient through a white
introducer, which has a clear side port :)
Dude, put a tegaderm on that site! (Why?)
http://www.castenholz.org/ptguide/special.htm
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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) – that’s the volume…
- and how well your patient’s arteries can squeeze : that’s the
SVR – the “systemic vascular resistance”…
PA lines are serious juju – they’re invasive, they’re tricky to place, they need
very serious care and feeding – in fact, they’ve 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! (www.icufaqs.org/PALinesApril04.doc)
10-2- Something that will make you look really smart.
(Or really antiquated :))
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 aline, multiplied by this, divided by that, aligned with the coefficient of
Hammerschmidt, over the square of the patient’s shoe size… and out come the
numbers. Cool!
Times are hard for the poor PA catheter
these days. Turns out they don’t really
make a big difference in outcomes, and
they’re used infrequently now in the
MICU. You’ll still see them occasionally
however, so you should learn how they
work and what they measure, and
actually that experience is very helpful
in mentally putting together the
components of blood pressure and
shock states.
Gone gone gone! No more green
dye outputs. Replaced!
Take a look at the ICON
noninvasive cardiac output
monitor:
http://cardiotronic.net/products/i
con
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 isn’t 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 MI’s - leaving them with a very low ejection
fraction - can live on the edge of cardiogenic shock much of the time.
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 can’t get up from the chair without
shortness of breath sometimes run in the low
teens.
Here’s the LV at the end of diastole – all full, ready
to go.
http://www.heart1.com/images/content/ejection1.jpg
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Here’s 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? That’s “pump”. So what happens if the pump
can’t pump?
http://www.heart1.com/images/content/ejection2.jpg
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 wouldn’t 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 (www.icufaqs.org/IABPFAQ.doc) – 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 patient’s blood
pressure rises, and if the system loosens up, the pressure falls – which is the cause of hypotension in
septic shock.
http://www.medicalillustration.net/Museum_images/images/arteries_runner.jpg
So the trick in diagnosing hypotension is to figure out: which of the three components is the problem?
There’s lots more on this subject in the PA-line FAQ.
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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. www.Icufaqs.org/ArterialLines.doc
Here’s one. It’s the same catheter as an
IV, usually a 20 gauge angiocath, inch
and a quarter, in the radial artery,
hooked up to a transducer.
http://www.zefon.com/medical/aline.htm
A “labile” blood pressure – an unstable one – needs constant monitoring, because… well, because it’s
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 didn’t think you were going to get to sit down in the ICU, did you? If you don’t 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 another of the three parts of the blood pressure, and
each kind of shock has a characteristic pattern of these 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-1’s (you have one
heart, that’s where they are), and beta-2’s, (you have two lungs, that’s 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
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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 isn’t the problem, it’s the “squeeze” that’s not right.
Nope nope nope: levophed is the
pressor of choice for sepsis
nowadays. We still use peripheral neo
as our first line pressor agent while
we’re getting central access, but after
that we change to noreipnephrine.
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 PA line 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 the circulating volume
squeeze the tank: apply the appropriate pressor to tighten up the arterial bed
kill the bugs: find the source, and give the appropriate antibiotics. (Note to early
responders: guys? Make sure you send blood cultures BEFORE YOU START ANTIBIOTICS!)
(quietly swears)
Nowadays there’s 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 they’re too tight, and the little arterioles
can’t get their supply – they’re 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 doesn’t 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”, you’ll
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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, isn’t 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 doesn’t work in septic
situations the way you want it to. Lately there’s 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 – it’s “chronotropic” – that is, it raises
heart rate, even at low doses, and because it’s often the only pressor
available for peripheral use, it is used in situations where it probably
shouldn’t be – although in a code, or near-code, you do what you have
to do to save a life. If there’s no option but to run a vasoconstrictive
pressor through a peripheral vein while the team is getting, say, a
femoral line placed – well, that’s what you have to do. Change over
quickly – the patient could lose an arm if the drug infiltrates!
Thank GOODNESS they got
away from the “dobutamine
in sepsis” thing.
There was a sort of, kind of,
maybe, sort of logic in there,
sort of, because it’s very true
that in severe sepsis you’ll
see severe myocardial
depression, meaning: the
pump doesn’t pump. I
remember a male patient of
about 20, otherwise healthy,
with a horrible sepsis, whose
cardiac output was
terrifyingly low. Still, given
the tachycardia these people
have, and the dangers of
applying a pure beta pressor
to them? Namely like maybe
VT/VF? It made NO sense. In
fact the cardiac output
usually recovers very rapidly.
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, what’s going to happen to
the tissues at the site? Why?
Regitine is the drug for this situation: it’s an alpha-blocker. What the docs will do is draw it
up in a syringe, and with a subcutaneous injection needle, they’ll infiltrate this stuff into the
tissues around the IV site, hopefully reversing the alpha effect of the pressor. Apparently it
works – I’ve only seen it done once or twice, but you might save someone’s 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 – it’s the right thing to do – but you need to make sure that
it’s in the right place. You’re using the line, it’s your responsibility. Once the patient gets to you, wherever
that line is: transduce it. You’ll immediately get lots of arguments about whether or not the number is
“real”, and all this, but that’s not the point. You’re trying to make sure that you’re not sending pressors
downstream, towards the leg, right? What would happen in that case? What if the line wasn’t in a vessel
at all – maybe in the peritoneal cavity? What then?
So – transduce the line. If it’s arterial – you’ll know! If it’s venous, you’ll know that too. Who cares if the
number is correct – as long as there’s a CVP waveform of some kind, and the mean pressure is about, say,
12, and not 60 – you’re 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”
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beta pressor. (Assuming you want to use a pressor at all. You don’t want to “whip” an already failing left
ventricle if you don’t need to – you use an intra-aortic balloon pump – another FAQ.)
You have 1 heart – that’s 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 can’t 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. (You’ll 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 – that’s 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 aren’t 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 occasionally.
At middle ranges: 300-600 mcg/minute – dopamine has beta effects – it increases heart rate and inotropy.
There’s 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, kick-everything”
pressor, hardly used except in codes and as a last-ditch in hypotension that’s 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 doesn’t work – the drill used to be: A-I-P for
symptomatic bradycardia: atropine, isuprel, pacing wire. Nowadays we use the Zoll pads.
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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. Here’s 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 patient’s 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
here.
Here’s the part that
spikes the bag…
and here’s the end of
the line, closest to the
patient…
and here’s a y-site
connector, where you
plug things in…
http://teach.lanecc.edu/nursingskills/iv/images/clampTubing.jpg
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 you’re 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 don’t want to hook up the syringe directly to the infusion port either – a drip running at 2.4 cc/ hour
isn’t enough to keep the lumen from clotting off – that’s what the flush is for.
So okay – you don’t want to use the y-connector… what to do?
12
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 they’re essential. Very useful.
Here’s just one…
And here’s a bunch of them connected together – a
“manifold”.
http://www.plastimedical.com/html/accessories.htm
Screw the manifold onto the end of the flush line tubing, and the other end onto the infusion port of the
patient’s 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 patient.
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 you’re looking
for.
Also – don’t 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 you’ve washed all the pressor out of it, and you’re
going to have to wait all over again for it to work, which means the patient will get hypotensive again…
22-2- Drug Rates:
Let’s talk briefly about rates. In almost every hospital in the universe, vasoactive drugs are delivered
based on the patient’s 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. It’s easy, and in practice, you’re titrating the drug for effect, right? So it
doesn’t really matter what dose technique you use, as long as you stay in the ranges in your policies.
Check them frequently!
13
Here’s a quick example of how it doesn’t 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 she’d 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 don’t 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 I’ve 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 I’m going to start at 100mcg instead. He has this look: “Ok, I’ll indulge the old nurse.
Poor old guy.”
An hour later, the lady’s heart rate has gone from 74 to 118. She’s 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 hadn’t read the intern’s textbook. 
23- Are there other vasoactives I need to know about?
We haven’t 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 don’t think there’s 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: it’s 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, you’ll 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 it’s 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 v-fib! Very cool!
-
Nitroglycerine (TNG) is used for controlling anginal symptoms and for acute blood pressure
control (it doesn’t 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 it’s
easier to pump it out, because the arterial tank is bigger - looser.
14
-
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 patient’s 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 halflife, 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 we’ve mostly gone to
octreotide for this situation, but it’s 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 patient’s pressure recovers.
The theory as I understand it (not very well), is that in sepsis the body gets into a vasopressin-deficient
state, which contributes to the systemic arterial vasodilation. I have to say that I’ve really been surprised
at how effective this stuff is – actually the really impressive part for me was how SVR recovers with this
drug. It’s 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 300’s, maybe. I have no clue why –
you’d think it would rise as the pressure did. Not until vasopressin came along did the numbers actually
start to reflect what you’d expect.
The other significant thing about vasopressin is that you’ll see your patient’s heart rate drop, sometimes
down from say, the 130s, to around 60 or 70. It may take a day or longer for the heart-rate effect to show
up, but blood pressure usually responds within an hour or so in my experience. This can make your team
nervous – we’ve seen some patients on vasopressing get into bradycardias in the 40’s, with serial EKGs,
troponins, much head-scratching… remind the team that it may be the drip. They’ll look at you as though
you’re mad, until the attending comes in and agrees with you. Then they’ll look at you as though you’re
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 don’t 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-hypo-pituitary, after a brain tumor was removed.
Didn’t make any ADH. So if he missed his DDAVP pill (used to be nasal spray, now I guess there’s a pill), it
was like Niagara Falls in his room until we could get it into him! So it’s good to know that there’s an
endocrine aspect to hemodynamic management too, although you don’t see it too often…
15
25- Why don’t we use the Trendelenburg position for hypotension any more?
Ok – which one is this?
And this?
http://www.denyers.com.au/versatility.html
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 isn’t, 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.
Don’t 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- Here’s a little Chart Thing for those who like them:
Condition  CVP/PCW  CO/ CI  SVR SV  Pressor to Use?  Receptor to Treat
Normals: 8-10/ 10-12
Sepsis:


Cardiogenic: +/- 
Hypovolemia:  
4-6/ 2-3
 
 
 
1000



80+/


Coffee!
Caffeine!
Neo, Levo, Vaso Alphas
Dobutamine?
Beta-1s  IABP?
Fluid or blood only?
16
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:
abcde-
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
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:
abcde-
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
B and d, except for the lawnmower
4- The three parts of a blood pressure are:
abcd-
pump, crackle, and pop
snap, squeeze, and Dopey
squeeze, pump, and volume
Huey, Looey, and Sneezey
5- Cardiogenic shock results from:
abcde-
pulmonary failure
a big MI
a low EF
a high EF?
B and C
6- Volume is measured with:
a- a CVP line
b- an arterial line
17
c- a foley catheter
d- a blood pressure cuff
e- feeling the inside of your patient’s mouth for moisture
7- Pressors are for:
abcd-
all shock states
some shock states
Only states where they’re allowed by law
Certain shock states, depending on what the cause is
8- How many adrenergic receptors do we think about?
abcd-
One
Two
Three
Eighteen
9- Pump is measured, numerically, using:
abcd-
cardiac output
cardiac index
pulmonary output
pulmonary index
10- Squeeze is measured with:
abcde-
a girdle
a PA line
a green dye output
SVR
PVR
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 it’s attached to
12- To antagonize a receptor is to:
a- make it angry
b- to – generally – decrease the activity of the organ it’s attached to
13- The pure alpha pressor that we use is:
abcde-
levophed
nipride
phenylephrine
dopamine
colace
18
14- The pure beta pressor that we use is:
abcde-
dopamine
dobutamine
milrinone
amrinone
saxamaphone
15- Vasopressin is:
abcd-
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- what’s an infiltration?
True or False:
17- All central lines should be transduced as soon as possible, to make sure they’re in the right
vessel.
18- All central lines should be transduced as soon as possible, to make sure they’re in the left vessel.
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…)