Adrenaline in Cardiac Arrest: Jim Manning

[@redrum776]

Great talk

[@kevrenshaw6177]

Really useful. Good talk. Thank you. Surprised no one has looked into this before.

[@tomriley5790]

Okay - here's where I see the logical hole in this reasoning. Peripheral Adrenaline improves ROSC and admission to hospital, but doesn't improve discharge or neurological outcome. By definition people successfully discharged from hospital must be admitted - so to me this suggests either adrenaline is intrinsically doing something that as well as increasing the chances of ROSC fails to improve/preserve neurological function (given that the patients it's making a difference to get admitted would otherwise be dead with no neurological function). Adrenaline is shown/believed to work by improving aortic arch pressure/coronary perfusion pressure which is rasied by peripheral adrenaline presumably "high dose peripheral" also led to a corresponding higher aortic arch diastolyic pressure (no evidence but seems reasonable given there is a dose-response relationship to aortic adrenaline) but with no improvement in hospital discharge/neurological outcome. You can improve coronary perfusion pressure/chance of ROSC with a smaller amount of intraaortic adrenaline. So with all the evidence presented here it seems to me that we can say the chance of ROSC correlates with intraortic pressure/CPP, that is increased by adrenaline peripherally and increased more by aortic adrenaline - but I don't see any evidence (presented) that suggests that intraortic adrenaline (albiet a smaller and more titrated dose) would not simply result in the same effect of increased ROSC but no improvement in neurological outcome/discharge from hospital - this would only be the case if the absolute dose of adrenaline in some way was important - i.e. it was in some way toxic to the brain, which seems possible - cerebral vasoconstriction/vasospasm, but is there any evidence for this. It's also possible that post ROSC care needs to be tailored in some way for those patients who obtain ROSC due to adrenaline, i.e. we're doing something wrong with them once they arrive in hospital to create the difference in eventual outcome. However I suspect that unfortunately the reality, and as far as I can see consistent with the evidence presented here is that cardiac muscle is more responsive to CPP and adrenaline after a periood of ischaemia than neurological tissue and therefore it's unlikely to make much of a difference to hospital discharge/neurological intact survival, in which case being able to titrate doses to a number on a monitor might be intellectually nice but ultimately pointless - unless anyone knows of a study that's been done (if not it would seem like one potentially worth doing - but hard to do).

[@jonathanerickson1543]

Including CPP monitoring, ultrasound, and somehow getting intra-aortic meds sounds like a recipe for success in the prehospital setting.

[@terrainc9140]

For critical access hospitals, communities with limited BLS ambulance crew, or morbidly obese, intra-aortic catheters might not work. It would be preferable if AHA would simplify the cardiac arrest algorithms to remove ineffective medications

[@capmedic]

Yeah, but then how are they going to make money selling cards?

[@tomasgimenez4592]

You mean it took sixty years for physicians to realize that the blood has to be moving for a substance to reach the intended destination??

[@nilsoncorrea8474]

Com todo respeito. Que viagem na maionese. Em larga escala nao é factivel de modo algum.

[@gabmor7779]

what about a central venous line? seems more standard and almost just as good?

[@tomriley5790]

He covered that in the talk - in an animal model intraaortic produced a larger increase in CPP than Central Venous.