Nitro vs Nipride - page 2
by braden74 23,841 Views | 15 Comments
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... Read More
- 0Dec 4, '02 by Tenesmabrenna: you are on the ball when you say that decreased afterload is beneficial in the setting of pump failure.... however dobutamine is a poor choice for improving SVR. In fact, it works mainly through beta-adrenergic inotropic support... you basically want to improve cardiac output by giving better squeeze (ie: increase their stroke volume)... the reason why SVR tends to drop with dobutamine is that it is a partial alpha agonist and in the setting of the hyper-adrenergic state acts as an alpha-antagonist thus increasing venous capacitance and dropping preload.... so i will use dobutamine to improve stroke volume/contractility and then if afterload is still felt to be too high then i would add nitro/nipride.... some studies now support natrecor (brain-type natriuretic peptide) for improved cardiac output and afterload reduction... another good med is milrinone (phosphodiesterase inhibitor) - unfortunately it has a few downsides compared to dobutamine (it is longer acting and therefore more difficult to titrate and can often drop the pressure too much).
now neo is great because it has almost pure alpha activity, but i would argue that in the septic patient levophed would be a far better drug.... the reasoning behind this: the septic patient tends initially to have a high cardiac output, but this is quickly replaced with a tired and weak heart requiring some inotropic support as well, hence the advantage of levophed... and most frequently tachycardia in the septic patient is usually due (when not attributable to arrhythmias) to either reflex tachycardia from fever or to hypovolemia from loss of vascular tone... so i will usually flood them with fluids and then add levophed and you will notice that their heart rate usually isn't that bad.... now of course if they are on chronic beta blockers and are in concomitant heart failure, it becomes a whole new ballgame...
the great thing about anesthesia is that when you are working on a critically ill septic CHF patient, you can try all those different drugs and really see the realtime changes/benefits/disadvantages... isn't anesthesia awesome? it is like your own chemistry set!!! (i realize this is kinda flippant - but i am taking this out of context of actual patient care)
- 0Dec 5, '02 by Brenna's DadTenesma,
Of course dobutamine can't be used alone in decreasing SVR, but I like it in pump failure because in addition to it's inotropic effects, it helps decrease SVR. However, I had been wondering for some time whether this improvement in SVR was mostly only a measured improvement and simply related to the improvement in CI (since SVR and CI are reciprical if BP remains the same.)
I'm also not sure if I am really getting your explanation concerning dobutamine and its alpha activity. You're saying it's a partial alpha agonist, which would cause the SVR to rise, but in hyper-adrenergic states, it acts as an alpha antagonist, causing SVR reduction? How interesting.
In regards to sepsis, I am not seeing many people who are needing inotropic support, unless of couse they have prexisting heart disease, in which case I agree with you that Levophed would be a better choice due to its Beta-adrenergic activity.
The majority of the septic hearts I see, can manage CI of 6-10 quite nicely for several days, until they either get better or develop MODS, at which point the Levophed and everything else is turned on.
That's why I don't appreciate Levophed nearly so much. In my clinical practice, I see the hyperdynamic phase of shock lasting for several days and if the patient is hypotensive during this time, I still prefer to use Neo. Again, mostly because the patient is either tachycardic (despite aggressive fluid resuscitation) or having an already high CI.
I will have to disagree with you that the septic heart is "quickly" replaced by a tired and weak one. At least this, is not what I am seeing in critical care.
- 0Dec 5, '02 by Tenesmabrenna:
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