Pulmonary Vascular Resistance

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VentdependenT

VentdependenT

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Does neosynephrine have any clinically relevant effect on PVR? How bout our other pressor friends with Alpha action?

What do you guys think of Nitric Oxide as a "weaning device" off inotropes in ye old tough valve/cabg patients? Does it make a difference if you really crank that stuff (80ppm vs 40ppm)? Does it make ANY DIFFERENCE in outcomes?
 
VentdependenT said:
Does neosynephrine have any clinically relevant effect on PVR? How bout our other pressor friends with Alpha action?

What do you guys think of Nitric Oxide as a "weaning device" off inotropes in ye old tough valve/cabg patients? Does it make a difference if you really crank that stuff (80ppm vs 40ppm)? Does it make ANY DIFFERENCE in outcomes?
Click to expand...

No response so far on a good topic to discuss.

Clinically relevant effect? Not in the normal or mildly compromised heart. It has the reserve to overcome a rise in systemic pressure without translating it back to the pulmonary circulation. I have had this argument many a time with a few CT surgeons who believe that alpha agonists, especially pure alpha agonists, necessarily directly impact PVR.

Levophed has both alpha and beta effects but you do not see significant changes in pulmonary vascular pressures unless you blast them at high levels, blast a failing heart, etc. It would seem make physiological sense as you do not want your lung vasculature and oxygenation to clamp down in a fight or flight situation with a big release of epi and norepi from the adrenals and nerve terminals, and I have yet to find a convincing study or article that shows that alpha agonists directly constrict the pulmonary vasculature at non-supraphysiologic levels.

Vasopressin has been shown in several animal studies to have mild pulmonary vasodilating effects at physiological levels, however.

Let the discussion continue.
 
i guess your question is: "is it dumb to use neosynephrine in a patient who needs a low PVR?"... the answer is no it isn't dumb, but maybe other pressors may be better.

nitric oxide ain't no weaning device

i have run NO on patients with acute huge PEs, heart transplants etc.... i am not sure NO had any real big effect --- might as well have used nitroglycerin.

and whoever argues with CT surgeons is a fool - it is a complete waste of time... they are convinced that they know what they are talking about (usually because the repeat like parrots the things they heard their mentors (trained in the 60s and 70s) scream at them)... i would recommend just letting them talk and talk, and then when they pause for a breath of air, just ask: "can you show me the literature that supports your antiquated concepts of pulmonary physiology?"
 
Well I don't remember the Swan numbers changing all that much when giving neo in the heart room. On occasion you can see a transient increase in the Pulmonary pressure (usually the sicker hearts) but it isn't very impressive.
 
Tenesma said:
just ask: "can you show me the literature that supports your antiquated concepts of pulmonary physiology?"
Click to expand...

There is the key question. I have very few inflexible CT surgeons that I work with, of the kind you see at most major academic institutions. Perhaps it is because they realize that they were only trained in one way and through even just loose association with each other, they have picked up on concepts that they were not previously exposed to.

Different CT surgeons also have had differing levels of involvement of anesthesiologists in postoperative cardiac critical care, so those that came from programs where we were intricately involved, tend to defer to our judgement, whereas those who did not tend to practice only what they were exposed to and try to control the intraoperative milieu to best suit their planned postop care.

Regardless, it's worth arguing from my perspective at least not to perpetuate myths.
 
Tenesma said:
i guess your question is: "is it dumb to use neosynephrine in a patient who needs a low PVR?"... the answer is no it isn't dumb, but maybe other pressors may be better.

nitric oxide ain't no weaning device

i have run NO on patients with acute huge PEs, heart transplants etc.... i am not sure NO had any real big effect --- might as well have used nitroglycerin.

and whoever argues with CT surgeons is a fool - it is a complete waste of time... they are convinced that they know what they are talking about (usually because the repeat like parrots the things they heard their mentors (trained in the 60s and 70s) scream at them)... i would recommend just letting them talk and talk, and then when they pause for a breath of air, just ask: "can you show me the literature that supports your antiquated concepts of pulmonary physiology?"
Click to expand...

Unfortunately NO gets thrown around like water with some of our CV surgeons. I haven't found it to be practical what-so-ever in the adult CV post op pulm-htn crew. It'll bring your swan numbers down but thats it.

I have no experience with prostaglandin infusions for pulm-htn.

Any of the surgeons using post-op sildenafil where you guys are at for pulm-htn?
 
NO--> seems to help prevent (notice the hedging) total RHF and get people off pump but for me that has always been in combination with Milrinone and vasopressin. So who knows what would have happened if it were not used. As hinted at earlier i doubt anyone could get CT surgeons to do a RCT on its use. I always find it funny in the ICU when the surgeons start out saying not to wean NO for certain PA pressures and after the pt has no improvement over a couple days and is ready to be extubated otherwise how quickly they change their thresholds.

Sildenfil was used a couple times preop by direction of the surgeon. Coming off PA pressures were lower but CPB use of phenylephrine and post CPB use of norepi seemed to be more. Have used it post op as well post as the pt heads out to the floor. Have also seen hypotension there as well limiting its use. I am not convinced either way just yet.
 
My view of PVR.

Who cares????

as long as:

1) not causing significant r to l shunt
2) enough CO to prevent allow oxidative phosphorylation

and if number 1 and 2 are not meant (very rare)...we do what we can to achieve 1 & 2.......and if we can't achieve 1 &/or 2...than it means that the patient is too sick to live.

there are just some things that we have no control over.
 
Another way to look at this issue is the ratio of increases of SVR to PVR.

The literature on this is actually pretty confusing. A great series of reviews in Seminars in CT and Vasc anesthesia last month on the Right Heart and Pulmonary Vasculature.

My take home: Weak literature that norepi's increase in SVR is greater in relationship to its increase in PVR when compared with neo. Vasopressin has become our pressor of choice as of late in folks with RV dysfunction/PVR issues.

So next, who wants to comment on the anesthetic management of the 40y/o F with severe pulm htn on flolan, bosentan, and sildenafil, 2L/min NC, presenting for EGD/colonoscopy?

Finally, I'd say our NO use in adults is at least 30% on traumatized lungs to improve V/Q matching. Anyone else using prostanoids/iSNP in place of iNO? If so, separating our RA vs LA lines anymore?
 
Gator05 said:
So next, who wants to comment on the anesthetic management of the 40y/o F with severe pulm htn on flolan, bosentan, and sildenafil, 2L/min NC, presenting for EGD/colonoscopy?
Click to expand...
Easy: Topical to throat and mouth then Propofol like every one else, just start gradually and stay light.
Have neo available.
And as the cardiologists often tell us: avoid hypotension and hypoxia 🙂
 
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So you'll knock down her preload, afterload and contractility all in one swoop?

Do you care about echo results? Volume status? Starting BP? Sats? ABG?

And why neo?
 
Gator05 said:
So you'll knock down her preload, afterload and contractility all in one swoop?

Do you care about echo results? Volume status? Starting BP? Sats? ABG?

And why neo?
Click to expand...
:laugh:
No you won't knock out anything if you know what you are doing.
The key words here are titration and slow.
On the other hand if you are in the big university hospital then here is what you do:
You tell the GI guy you need sometime to get her ready for the procedure, you float a PA catheter and place an A line, you also get the bypass machine ready and cannulate the femoral vessels just in case. You have the following drips ready:
Epinephrine, Norepinephrine, Dobutamione, Dopamine, Vasopressin.
You place a consult to the transplant team to see if we could give her a new heart and lungs before her impending endoscopy.
You correct her volume status according to her PAWP.
You start Dobutamine and optimize the cardiac index.
You take her to the hyperbaric chamber and hyper oxygenate for 1 hour.
After all these elements are covered you proceed with Propofol infusion.
 
Actually, we just used a little ketamine and versed. 🙂

But, and I think importantly, we'd thought about all that you'd mentioned. Maybe just for teaching/thinking purposes.
 
Damm Plankton, I liked that response! I wanna git somma dat! Regards, ----Zip
 
Planktonmd said:
:laugh:
No you won't knock out anything if you know what you are doing.
The key words here are titration and slow.
On the other hand if you are in the big university hospital then here is what you do:
You tell the GI guy you need sometime to get her ready for the procedure, you float a PA catheter and place an A line, you also get the bypass machine ready and cannulate the femoral vessels just in case. You have the following drips ready:
Epinephrine, Norepinephrine, Dobutamione, Dopamine, Vasopressin.
You place a consult to the transplant team to see if we could give her a new heart and lungs before her impending endoscopy.
You correct her volume status according to her PAWP.
You start Dobutamine and optimize the cardiac index.
You take her to the hyperbaric chamber and hyper oxygenate for 1 hour.
After all these elements are covered you proceed with Propofol infusion.
Click to expand...

HAHAHAHAHAHAHAHAHAHAHAHAHAHAHAHA

How true, how true.
 
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