No Beta Blocker for Heart Transplant?

[tniuqs]

Following this thread, frankly a bit confused....why exactly would one need to use Beta Blockers or Calcium channel blockers for a transplant patient in the first place? A run-away Tachycardia or Hypertension is a rarity I would think in this situation, personally I would look to other causes like the "root" cause of this senario..... using either drug "could" really comprimise this complex type of patient.

cheers

[fiznat]

While I admit I dont know much about heart transplants, it seems reasonable to me that tachycardia could be a common problem with these patients being that they no longer have the ability to control heart rate through parasympathetic activity. Heart rate in these patients is completely controled by levels of sypmathetic tone, which in many cases can get extrememly high. Beta blockers would do their part to limit this sympathetic tone, thus controlling heart rate through the only system available to do so.

Of course we always look at causes of a presenting problem, but often times these things are not all that obvious and we are resigned to treating only S+S. Beta blockers would serve well in this case.

[AZCEP]

Check the link I provided earlier.

Excess sympathetic discharge occurs due to the body trying to compensate for the progressive heart failure that leads to the transplant. Once the transplant is done, the adrenal medulla is still producing an excess amount of catecholamines. The excess causes the new, presumably healthy, heart to run with a moderate tachycardia. It also creates a mild hyptertensive state.

[Spock]

Darn but don't you folks come up with great questions. We don't do transplants at my hospital (thank God) so I went to Cardiac Anesthesia fourth Edition by Kaplan page 994-995. Cardiac denervation is an unavoidable consequence of heart transplantation. Long-term studies indicate that reinnervation is absent or only partial at best. Denervation does not significantly change baseline cardiac function but it does alter the cardiac response to demands for increased cardiac output. Normally, increases in heart rate can rapidly increase cardiac output but this mechanism is not available to the transplanted heart. Heart rate increases only gradually with exercise and this effect is mediated by circulating catecholamines. Increases in cardiac output in response to exercise are instead mostly mediated via an increase in stroke volume. Therefore, maintenance of adequate preload in cardiac transplant recipients is crucial. Lack of parasympathetic innervation is probably responsible for the gradual decrease in heart rate after exercise seen in transplant recipients rather than the usual sharp drop.

Denervation has important implications in the choice of pharmacologic agents used after cardiac transplantation. Drugs that act indirectly on the heart via either the sympathetic (ephedrine) or parasympathetic (atropine) nervous systems will generally be ineffective. Drugs with a mixture of direct and indirect effects will exhibit only their direct effects. Thus agents with direct cardiac effects (epi or isuprel) are the drugs of choice for altering cardiac physiology after transplantation. However, the chronically high catecholamine levels found in cardiac transplant recipients may blunt the effect of alpha adrenergic agents as opposed to normal responses to beta adrenergic agents.

So, (my analysis) beta blockers will work although if you use labetelol you would not get the alpha effect from it (labetelol is non-selective beta and alpha). Atropine won't work normally if at all. Not sure that this helps. I have often thought this would make a good article for a journal such as JEMS but I don't have the necessary expertise to write it. I'm going to suggest this to a fellow CRNA that does transplants at another hospital in our city. He is also active in EMS and might be interested in writing it.

Great topic.

Live long and prosper.

Spock

[itku2er]

I love this post I am learning alot and looking up alot of things by googling things everyone says

THANKS 678 for bringing this topic the heart and the brain have always facinated me

later

Terri

[tniuqs]

Darn but don't you folks come up with great questions. We don't do transplants at my hospital (thank God) so I went to Cardiac Anesthesia fourth Edition by Kaplan page 994-995.

Heart rate increases only gradually with exercise and this effect is mediated by circulating catecholamines. Increases in cardiac output in response to exercise are instead mostly mediated via an increase in stroke volume. Therefore, maintenance of adequate preload in cardiac transplant recipients is crucial.

Firstly great post very consise explanation, thanks for doing the leg work.

So extrapulating from your post and I suspect cut, copy, paste..... from Kaplan.

Preload and adequate circulating volume would be of key significance a fluid challenge may be the "best first" and conservative choice for a tachycardia.

Lack of parasympathetic innervation is probably responsible for the gradual decrease in heart rate after exercise seen in transplant recipients rather than the usual sharp drop.

Pmhx may be a very serious impact (ie What was the patient doing prior to arrival? )

Could an analgisia or a benzo be a better option?

I have "anecdotally" observed an SVT suddenly convert to NSR with the use of fentynyl and just prior to elective cardioversion in an ICU setting (applause was heard from the crouwd) the explanation being a reduction in the circulating catacholamines.

It is logical Mr Spock.

So quick off the mark beta blockers "could crater the patient" (due to the delayed response of the transplanted heart?) dunno?

Denervation has important implications in the choice of pharmacologic agents used after cardiac transplantation. Drugs that act indirectly on the heart via either the sympathetic (ephedrine) or parasympathetic (atropine) nervous systems will generally be ineffective. Drugs with a mixture of direct and indirect effects will exhibit only their direct effects. Thus agents with direct cardiac effects (epi or isuprel) are the drugs of choice for altering cardiac physiology after transplantation. However, the chronically high catecholamine levels found in cardiac transplant recipients may blunt the effect of alpha adrenergic agents as opposed to normal responses to beta adrenergic agents.

So direct adrenergics are the best choice with the medication route (I haven't seen Isuprel on the Cars for quite some time) but treating hypotension 'a much more likely senario" I suspect.

So, (my analysis) beta blockers will work although if you use labetelol you would not get the alpha effect from it (labetelol is non-selective beta and alpha). Atropine won't work normally if at all.

Not sure that this helps.

Yes it does.

I have often thought this would make a good article for a journal such as JEMS but I don't have the necessary expertise to write it.

Disagree, you know how to do "cut to the chase" research to be certian.....go for it!

[678 Responding]

Thanks a lot everyone for your input! I really appreciate it. I'm starting to understand it more and more each time I read the posts. I couldn't find the answers to save my life, thanks again!! I'm full of stumping questions, but the more difficult ones, everyone needs a little help once in a while. Hehe.

Stay safe!

[itku2er]

Thanks a lot everyone for your input! I really appreciate it. I'm starting to understand it more and more each time I read the posts. I couldn't find the answers to save my life, thanks again!! I'm full of stumping questions, but the more difficult ones, everyone needs a little help once in a while. Hehe.

Stay safe!

Hey 678

I have learned from this one too....thanks for sharing it

SO what is the next question :?: :?: :?:

later

T

[678 Responding]

How about the next powerball lottery numbers?