Ok I have seen this comparison more than once as a potential question during interviews. I have been looking over the two drugs and also going on what I have been taught. I was wondering if anyone has anything to add to the difference between the two drugs. What I know is
Nitroglycerin has more effect on Venous dilation and less on Arterial dilation than Nipride. Nitroglycerin has more effect on coronary artery dilation while Nipride has more effect on peripheral dilation.
If anyone has more info to add on this I would like to hear it.
In my CT ICU expereince, I am not a CRNA, but I have seen NTG used to reduce pulm HTN too. I think, if I remember correctly, nipride can cause a tachycardic effect as well.
Nitro is still pretty routine in CABG post-op, we always ran it at 33mcg/min for the first 24 hrs or so, then wean to ismo po. We used to use nipride pretty routinely, but then went to cardene, and occassionally esmolol. Now, since people are extubated so much earlier, we get a dose of lopressor into them asap post-op, also helps to ward off post-op a-fib. Usually post-op HTN is due to awakening or pain, so keeping them sedated on the edge of spontaneous breathing has been helpful.
I think dobutamine is my fav drug for pump failure, if there is enough systemic vasc resistance. Some of our docs swore by neo for low SVR, and others swore it killed the kidney's. Personally I like neo.
I think the biggest thing in my cardiac expereince is knowing when you have stepped over treatment, and are now treaing the treatment effects. Like when dopa is run at 15 mcg/kg/min and then nipride is started...hello, try turning down the dopa first! Less is always more.
Last edit by hoolahan on Dec 2, '02
svr is decreased because of dobutamines direct effect, but also at the same time remember that SVR is a purely calculated number (in which cardiac output plays a big role)... i am sorry i wasn't more clear on dobutamine.... like i said it is a complicated little molecule.... its beta- activity is clear, however it can get annoying regarding its alpha activity... there are cardiac alpha-1 receptors that respond by increasing inotropy on top of its cardiac beta activity, peripherally it is a partial alpha agonist and therefore binds to the alpha receptors.... however those alpha receptors would much prefer being bound by norepinephrine for improved stimulation, but once dobutamine binds it acts as competitive antagonist to norepinephrine (it isn't letting norepi into those receptors properly) and thus actually will lower your body's vascular tone even though your body is pumping out norepinephrine.... here is an example: you take a healthy resting human body and inject dobutamine, besides inotropy you will notice that their blood pressure slowly trends upwards.... you take somebody in an adrenergic state (septic, myocardial infarction/ischemia, traumatic), and you will see the pressure trend downwards... does that make sense?
people with sepsis: sepsis is a systemic reaction to toxins that afffects a lot more than just your vascular tone - have you noticed how peoples mental status changes when they become septic (even with a perfectly normal blood pressure - by the way, the definition of sepsis doesn't include hypotension - if you see hypotension then that becomes septic shock)? so if sepsis can alter mental status, what do you think happens to the heart? the tachycardia is usually due to hypovolemia and loss of vascular resistance, and trust me that "aggressive fluid resuscitation" is usually never aggressive enough. in the septic shock the body responds by increasing cardiac output, and the only way it can do so is by increasing heart rate, as i can guarantee you that their stroke volume can't keep up (3 reasons: ****** preload, short end-diastolic filling times because of their heart rate, floppy heart because of the effects of sepsis - if sepsis can hurt blood vessels it sure can hurt the inside of the heart which is a continuation of those blood vessels).... now why not increase inotropy (squeeze) so that you can increase their Stroke Volume??? you will quickly notice that their tachycardia will improve because you are then able to maintain their cardiac output with inotropy instead of chronotropy.... and by the way, tachycardia in of itself will create a vicious cycle of increasing cardiac output, because of the ever increasing oxygen demands of the myocardium.
for a long time levophed (norepi) was known to "leav'em dead"... but that misconception is due to the fact, that it was often used as a last ditch effort in the failing septic patient... there is more than enough literature out there right now that supports levophed as a primary agent over neosynephrine... now don't get me wrong, I love neo and used it a lot in the OR, but in the ICU i (as well as the other ICU docs) gravitate towards levo
just out of curiosity... what specialty of ICU docs runs your ICU?
Last edit by Tenesma on Dec 5, '02