Nitro vs Nipride

All I can add is both act via stimulation of guanylyl cyclase resulting in smooth muscle relaxation. In post-op hearts, NTG is for inc. coronary blood flow and SNP is for afterload reduction

You're both right, and braden, you can throw this in if asked in an interview--

Nitro is also used effectively in reducing post-CABG coronary vasospasms.

I am glad that somebody asked this question because I was looking over the same drugs plus a few more and it has helped me compare the two. I would like to add a few to the list if nobody minds.

Dopamine versus Dobutamine(what kind of situations would warrant one over the other etc.

Also, what kind of drips are being used on CABGs now. I see alot of neo, epi, nitro, cardene etc I know there is more but I can't think of them right off hand.

Has anyone seen people go into pulmonary edema from Cardene without a past history of CHF?? Speaking of pulmonary edema versus CHF. Can you have PE without ever having CHF?? thanks.

Tia

Another distinction, is cyanide posioning related to nipride, and metHGB.

The metabolite of Nipride is a toxic substance, and will bind Hemoglobin causing decreased oxygen carrying capacity, reflected by decreased sats. The reversal agent is methylene blue, which knocks the metabolite off.

Craig

for Tia:

dopamine and dobutamine are 2 very different drugs despite very similar names... and are therefore used for totally different situations.

dopamine has dopaminergic, beta and alpha agonist activity

and is the poor mans pressor... i prefer phenylephrine or norepi (levophed).... at "renal" dose it does improve natriuresis (urine output), but if the patient is going into renal failure it does nothing to improve outcome (yeah they might pee a few more drops, but that is far from meaning the kidney is rescued)

dobutamine is rather complex: it is a synthetic catecholamine with beta adrenergic agonist activity, but it also has "partial" alpha agonist behavior which means it can increase systemic vascular resistance in a non-catecholamine state, if the body is in a catecholamine state (release of systemic/endogenous norepinephrine) then it will antagonize norepinephrine and actually behave as an alpha antagonist... i mainly use it for extra squeeze (cardiac output improvement if there is pump failure)

cardene is nicardipine - a calcium channel blocker... there are enough studies to show that calcium channel blockers actually increase mortality outcomes in heart failure and infarction patients.... i therefore don't use calcium channel blockers in patients with acute heart failure, but i wouldn't be surprise if people did go into pulmonary edema... the reason why is that it acts as a negative inotrope (weakens the heart further) when you need the opposite effect- which outweighs its good afterload reduction

can you have pulmonary edema (by the way PE is an abbreviation for pulmonary embolus....) without CHF??? sure you can... you can have non-cardiogenic pulmonary edema or negative pressure pulmonary edema...

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.

Adding to what Tenesema had to say about calcium channel blockers and heart failure. Calcium channel blockers maybe okay to use with diastolic dysfunction, but not systolic dysfunction. You need to know what type of heart failure you are looking at by looking at EF etc before knowing which combination of drugs to use. Like Tenesema said because of the negative inotropic effects you would not want to give a drug which would furthur reduce contractility such as in systolic dysfunction which causes heart failure.

This kind of turns into an interesting case and I really wonder if it was the calcium channel blocker alone that was causing the pulmonary edema. When my patient started having symptoms of pulmonary edema we drew cardiac enzymes and did an echo. Troponin was slightly elevated but the echo showed no abnormalities and her ejection fraction was normal. Presssures within the heart were all normal also. I go back to work on Friday I will have to check and see what happened while I was gone. Thanks everyone for responding.

tia

You comments on dobutamine are interesting Tenesma. I had aways learned that dobutamine actually decreased SVR somewhat, which is why it is so good for pump failure (ie. decreased afterload). My clinical practice always backed this up as well.

I must reseach this some more.

Concerning, Neo, it has become a favourite drug of mine as well, especially in the spetic patients I see presently. Nothing like its pure alpha effects, increasing BP while decreasing HR. So much better than dopamine, which thankfully I am beginning to see much less in this class of patients.

brenna: 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)

Tenesma,

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.

brenna:

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: shitty 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?