Titrating and Bolusing

Specialties MICU

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So I am a new nurse about 2 1/2 months into an ICU internship program and while I've worked with some wonderful preceptors who are teaching me tons of great info, one area of ICU nursing that I'm still extremely uncomfortable with is managing drips. Just to preface, at my hospital ICU nurses have MD orders to titrate/bolus certain drips to desire effect (ICP, RAAS, MAP etc.) However, other than a card that has min and max rates (sometimes followed by "or higher") The amount a rate is changed or dose of a bolus is at the nurse's discretion. While I am starting to pick up some concepts, I am still miles away from being at the point where I'm not running to my preceptor every time so and so's VS are going beserk to find out which drips i need to bolus/decrease rate/increase rate and by how much??? When I ask them to explain I usually get the response that its something that comes with experience or it just depends on the patient. I am in NO WAY faulting them for not sharing the secrets of titration/bolusing as I realize that it is a complex issue that depends on a wide variety of factors that can't be explained properly during the occasional downtime we may have on this busy unit. So my question is does anyone have a reference/book they recommend for brand new nurses on this subject. The information I find in my nursing school books/the internet just doesn't cut it. I really want to become a competent nurse who practices safely and I am willing to do whatever it takes. I realize that this skill is truly built through experience, and I don't expect a book to make me an expert, I just need some basics to start with and build upon. Thanks all :-)

Let's not leave out Neosynephrine in the talks. If you're concerned about heart rate, go with Neo. No beta, pure alpha agonist. Not sure if you've had experience with that drug yet.

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I have seen neo, but haven't had a chance to really work with it yet. And yes, they recently changed to weight based dosing for levo so many of the nurses are getting used to that (many of my preceptors have had a calculator on hand to calculate the mcg/min because that is what they are all still used to). We eventually did hook up a CVP monitor and on avg he was~12 and the pt. had terrible ascites (liver failure) so the doc had put in some sort of abdominal drain (i forget what he called it) which we were replacing every 2 L drained with 25 g of albumin. By the end of the 24 hr period we had drained ~8L from the abdomen (which had pharmacy upset because they said we shouldn't be pulling off more than 6 L, but the docs goal was 10L before clamping -- we called to clarify b/c pharmacy was reluctant to give us anymore albumin but the doc confirmed that 10L would be fine) We also had D10 IVF running but I can't recall the rate (I want to say 150 ml/hr), because when they had turned off the D51/2NS drip our next blood glucose was 22. The pt. had gotten dialysis a couple of times during day shift since his UO = 0 for 2 days (i think they pulled ~500 mL the first day and ~1000 mL the second day), but not sure of the details other than that. The pt was ventilated and I believe the setting were A/C with TV = 600 R= 14 PEEP = 5 and FiO2 60%, but his RR was was 30s-40s which we were trying also get under control with our sedation drugs. We were doing Q3H x 3 ABGs which initially showed metabolic acidosis, we gave bicarb, and the next ABG showed respiratory alkalosis. I thought that this was because of his respiratory compensation for the metabolic acidosis, but the doc said something about having 2 separate unrelated processes going on (he was kind of hard to understand so maybe some of you can help me fill in the blanks here).

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You mentioned that the levophed was at 0.5mcg/kg/m. I've never heard of weight-based dosing for norepinephrine. Our max is ~30mcg/m. We see levophed used as a 1st line pressor mostly in sepsis. You're right about the alpha effects, and it does have some beta-1 but not beta-2 properties (which makes it more desirable than epinephrine in some cases).

It's something that some facilities do. I've never worked with weight based norepi dosing and I don't think I would like it! I've dosed it so long in mcg/min! Our "max" norepi dosage is 90mcg/min.

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I have seen neo, but haven't had a chance to really work with it yet. And yes, they recently changed to weight based dosing for levo so many of the nurses are getting used to that (many of my preceptors have had a calculator on hand to calculate the mcg/min because that is what they are all still used to). We eventually did hook up a CVP monitor and on avg he was~12 and the pt. had terrible ascites (liver failure) so the doc had put in some sort of abdominal drain (i forget what he called it) which we were replacing every 2 L drained with 25 g of albumin. By the end of the 24 hr period we had drained ~8L from the abdomen (which had pharmacy upset because they said we shouldn't be pulling off more than 6 L, but the docs goal was 10L before clamping -- we called to clarify b/c pharmacy was reluctant to give us anymore albumin but the doc confirmed that 10L would be fine) We also had D10 IVF running but I can't recall the rate (I want to say 150 ml/hr), because when they had turned off the D51/2NS drip our next blood glucose was 22. The pt. had gotten dialysis a couple of times during day shift since his UO = 0 for 2 days (i think they pulled ~500 mL the first day and ~1000 mL the second day), but not sure of the details other than that. The pt was ventilated and I believe the setting were A/C with TV = 600 R= 14 PEEP = 5 and FiO2 60%, but his RR was was 30s-40s which we were trying also get under control with our sedation drugs. We were doing Q3H x 3 ABGs which initially showed metabolic acidosis, we gave bicarb, and the next ABG showed respiratory alkalosis. I thought that this was because of his respiratory compensation for the metabolic acidosis, but the doc said something about having 2 separate unrelated processes going on (he was kind of hard to understand so maybe some of you can help me fill in the blanks here).

Neo can be a great drug in certain times but it's not really a *great* drug to use as a stand alone pressor because it can cause a reduction in cardiac output. Neo is really good in helping to correct some refractory hypotension and it helps to correct that SVR. It's also frequently given IVP or run in the background in the OR to help counteract the effects of afterload reduction from propofol and the volatile anesthetics.

It sounds like your patient overall was just a hot mess. He definitely sounds like candidate for SLED. I certainly hope they weren't doing HD with him considering the dosage of pressors and his continued hypotension despite interventions. Was your patient edematous and 3rd spacing?

You mentioned that your patient had a RR rate in the 30's and 40's and he's got a Vt of 600......What happens to your blood gas when you are tachypenic? What would you expect to see your Ph and your pCO2 do? Any idea on what your serum CO2 was? I am not saying that this is the explanation for your gas but that it's one *conceivable* portion of it.

Just a few thoughts! :twocents::twocents:

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Specializes in ICU.

One other thing to consider if you find yourself going up & up on pressors is your pt's pH. Consider getting an ABG. Pressors don't work well with acidotic pts.

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One other thing to consider if you find yourself going up & up on pressors is your pt's pH. Consider getting an ABG. Pressors don't work well with acidotic pts.

And bicarb, IVP or by drip, isn't going to save the patient. If they need a bicarb drip for days, chances are they're probably pretty far gone. It definitely has its place, don't get me wrong.

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Specializes in ICU.
And bicarb, IVP or by drip, isn't going to save the patient. If they need a bicarb drip for days, chances are they're probably pretty far gone. It definitely has its place, don't get me wrong.

Yup! When their lactic acid is 12.4, that's not a good thing:eek:. Bicarb pushes or drips or THAM or CRRT might extend the dying process, but the ending will likely be the same.....deceased. If you have a "reasonable" patient who suddenly develops metabolic acidosis/elevated lactic acid levels, then the reasonable person might want to consider ischemic bowel or some other ischemic process. If, on the other hand, you have your standard 217 year old CHF (EF 13% x 15 bedridden years)/COPD/MI/CABGx5/DM/... ICU patient who is maxed on half a dozen pressors who decides to spike a lactic acid level and crash their BP, then it might be time to "Say goodnight, Gracie". Then it's time to convince the pt's family. Good luck!

Back to the original topic of titrating vs bolusing.....every facility is likely different in terms of the reasonable scope of practice & expectations. If you're an ICU RN taking care of a pt with a sucky BP, starting a pressor, then you might initiate the pressor at a rate higher than the "norm." For Levo, my facility normally runs 0.02 - 0.20 mcg/kg/min. If a certain person is starting a Levo drip on a pt with a BP of 40-50 systolic requiring pressors, that person might initiate the drip at 0.3 - 0.4 mcg/kg/min, then RAPIDLY decrease the drip rate once the BP starts to increase (best evaluated on pts with arterial lines).

I, on the other hand, always conform to all applicable facility guidelines regarding drip rates at all times, no matter the circumstance. RIGHT??

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The TV was decreased to 400 (i gave you his pre-ABG settings).... And yea everyone involved knew this pt. was probably not going to survive very long, we were just doing everything until the family could make a decision. Just found it to be a great learning experience with so much going on, and I really want to start understanding the objective/goals of treatments and what types of outcomes to expect from all the interventions. I really have enjoyed reading everyone's responses because it challenges me to look at the bigger picture. Thanks all for helping me think through this :-)

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