Understanding cardiac gtts - page 2
I could really use a little direction... I work in the SICU but posted here as it has specific regard to my cardiac pts. I have been trying for some time to really understand the gtts that we use... Read More
0Jul 28, '12 by RNerd81, BSN, RN@belgianrn
the evidence for "renal dose dopamine" is clearly negative with regard to mortality and renal failure...there is no conclusive evidence that it has benefit in either of these areas. however, there is evidence that it directly dilates the renal arteries and can improve renal perfusion. this may produce increased urine output. there is also some inotropic effect (even at renal doses) in certain patients, which may also increase urine output. so for patients in whom an increase in urine output and renal perfusion is sought, dopamine may be used. see the anzics trial ([color=#0a0905]lancet. 356(9248):2139-43, 2000 dec 23-30), or this meta-analysis:[color=#0a0905]annals of internal medicine. 142(7):510-524, april 5, 2005. this is a very select patient population, however.@squirtle
as you can see, even in medications that have been around for some time, there is still debate as to efficacy and place in therapy. another example is the current debate between dopamine and norepinephrine for cardiogenic shock (see new england journal of medicine,[color=#0a0905]362(9):779-89, 2010 mar 4).
0Jul 28, '12 by BelgianRNRNerd81 what's the point in increasing renal perfusion if it doesn't stop the patient from going into renal failure or from dieing? Especially if you look at the safety of the drug you're using. In very select patients it could make the numbers of my fluid balance look better, but that's about all it does.
0Jul 28, '12 by RNerd81, BSN, RN@BelgianRN Two populations that may benefit are those in which we expect more difinitive therapy for heart failure: pre-transplant and LVAD. In these patients, improved diuresis in the short term may prepare them for improved outcomes after surgery. The concept is similar for long-term inotropic support (such as home-going milrinone or dobutamine)...these drugs do nothing to improve mortality, and may even increase mortality, but as a bridge to transplant, they have use...because our goal actually isn't mortality (with their current heart).
0Aug 5, '12 by sharifi9879I learn you on formula for any dosage calculation.
step 1: convert the unit of measurment of both doctor order and medication as same.
for example: 10 micro/kg/min dopamoin (medication shape= 200 mg/5ml)
for order= 10 / 1000= 0.001 mg/kg/min or for medication = 200 * 1000 = 200 000 micro
note: unit of measurment must be same.
step 2: use 100 cc normal saline as diluent
step 3: if patient weight is important, multiply pt weight on order. (60 * 10=600)
step 4: calculate the amount of solvent that contain ordered dose.
200 000 100 cc N/S
600 X= 600*100/200000
step 5: multiply X on 60
(60 000/200 000) * 60 = Y
Y is the number that you can use for gtt/min or cc/hr
0Aug 7, '12 by ozarkmommadobutamine is used to increased contractility, not increase bp!! it treats chf...
0Aug 12, '12 by 8jimi8ICURNQuote from squirtleIf you want to understand the drugs, study the pharmacokinetics. Especially the method of action.I could really use a little direction... I work in the SICU but posted here as it has specific regard to my cardiac pts. I have been trying for some time to really understand the gtts that we use on a daily basis and how they act on the body but I seem to have some sort of block in my head when it comes to comprehending the information presented to me Sometimes I feel like I am back in school trying to make sense of algebra- something I was never able to do. :icon_rollI am going to try and explain my confusion in hopes that someone may have an idea of how I can better learn this material. I have bought several books, have bookmarked several websites and something just doesn't click. As an example, I was reading about dobutamine and dopamine today. I don't truly understand the differences between the two. The more I read, the more confused I become. I try to understand vaso- renal dosing vs bp control and become confused by what I read. Why do we like levo in some pts and epi in others? I am not really looking for an answer to those questions specifically- but perhaps a suggestion on a book or some teaching material that goes back to basics and will help me understand why certain drugs act a certain way. Thank you for any direction you can give me.