Pressors and Vasoactives



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!

1- What is a pressor?

2- What is shock?

3- Are there different kinds of shock?

4- What are the three parts of a blood pressure?

5- What does “pump” mean?

6- What is “inotropy”?

7- What about “volume”?

8- What’s “crystalloid”?

9- What is “squeeze”?

10- How does this relate to shock?

10-1- PA Lines

10-2- Something that will make you look really smart!

(Or really antiquated :))

11- Which shock state reflects a “pump” problem?

12- What is “ejection fraction”?

13- Which shock state reflects volume?

14- Which shock state reflects arterial squeeze?

15- What measurements do we use at the bedside for treating shock states?

16- How do pressors fit into the treatment of shock states?

17- How do pressors work on receptors?

1. - Agonizing receptors

2. - Antagonizing receptors

3. - SVR

18- How are other shock states treated?

19- Are pressors used to treat hypovolemic shock? An important point. Another one.

20- What about cardiogenic shock?

21- What other pressors are there?

22- What basic considerations should I keep in mind when using these drugs?

22-1- Setting up the drips.

22-2- Drug rates.

23- Are there other vasoactives that I need to know about?

24- How do we use vasopressin?

25- Why don’t we use the Trendelenburg position for hypotension anymore?

26- 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 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? Quick-and-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.

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?



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. (PulmonaryEmbolism.doc)

Hmm – think we could measure this “LV inotropy”?



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?

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?



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…



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 Swan-Ganz 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?)



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! (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 a-line, 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!

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.



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?



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 (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.



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.

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. 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.



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 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.

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 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!

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” 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.

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…



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?

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”.



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!

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.

- 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 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 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…

25- Why don’t 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 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 4-6/ 2-3 1000 80+/- Coffee! Caffeine!

Sepsis: ( ( ( ( ( ( Neo, Levo, Vaso Alphas

Cardiogenic: +/- ( ( ( ( ( Dobutamine? Beta-1s ( IABP?

Hypovolemia: ( ( ( ( ( ( Fluid or blood only?

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:

a- drugs that press on things

b- pills that raise blood pressure

c- pills that lower blood pressure

d- 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:

a- how you feel when you come to work in the MICU

b- when your patient has low blood pressure

c- when she has high blood pressure?

d- 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:

a- pulmonary failure

b- a big MI

c- a low EF

d- a high EF?

e- B and C

6- Volume is measured with:

a- a CVP line

b- an arterial line

c- a foley catheter

d- a blood pressure cuff

e- feeling the inside of your patient’s mouth for moisture

7- Pressors are for:

a- all shock states

b- some shock states

c- Only states where they’re allowed by law

d- Certain shock states, depending on what the cause is

8- How many adrenergic receptors do we think about?

a- One

b- Two

c- Three

d- Eighteen

9- Pump is measured, numerically, using:

a- cardiac output

b- cardiac index

c- pulmonary output

d- pulmonary index

10- Squeeze is measured with:

a- a girdle

b- a PA line

c- a green dye output

d- SVR

e- 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:

a- levophed

b- nipride

c- phenylephrine

d- dopamine

e- colace

14- The pure beta pressor that we use is:

a- dopamine

b- dobutamine

c- milrinone

d- amrinone

e- saxamaphone

15- Vasopressin is:

a- run at a rate of 0.4 units per minute

b- run at a rate of 0.04 units per minute

c- run at a rate of 4.04 units per minute

d- 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…)

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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!

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:

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.

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.

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