Adrenaline in Cardiac Arrest: Jim Manning

#cardiacarrest #adrenaline #healthcare
Jim Manning presents the how and why of adrenaline in cardiac arrest.
The use of adrenaline in cardiac arrest resuscitation has been popular since the 1960s.
Laboratory studies and anecdotal experience showed improved rates of return of spontaneous circulation (ROSC) with the use of adrenaline at small dosages. This led to the widespread adoption of adrenaline administration during cardiac arrest into every resuscitation guideline for decades to come.
Extensive laboratory studies characterised the beneficial physiological effects of adrenaline during cardiac arrest and closed-chest cardiopulmonary resuscitation (CC-CPR). Adrenaline administered during CC-CPR results in peripheral arterial vasoconstriction that raises the aortic pressure. Particularly during the relaxation phase of CC-CPR.
This increase in aortic pressure results in an increased aortic to right atrial pressure gradient that drives blood flow to the myocardium during CC-CPR. This pressure gradient is known as the coronary perfusion pressure (CPP) and this correlates with ROSC in laboratory investigations and clinical studies.
During the 1990s, the use of “high-dose” adrenaline showed increased rates of ROSC compared to “standard-dose” adrenaline. However, larger doses of adrenaline did not result in improved survival.
Recent meta-analyses have raised serious questions about the value of adrenaline. Notably, showing a benefit for achieving ROSC but no clear evidence of improved long-term survival.
Controlled clinical trials to address this question are now underway. However, there is another important issue that needs to be addressed: the “route” of administration.
With the growing interest in endovascular resuscitation, the use of intra-aortic adrenaline titration offers a means of rapidly and effectively delivering adrenaline to peripheral arterial effector sites while providing arterial pressure and CPP monitoring to guide titration of adrenaline doses to achieve an optimal hemodynamic effect while avoiding excessive adrenaline doses.
codachange.org...

[@redrum8665]

Great talk

[@kevrenshaw6177]

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

[@jonathanerickson1543]

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

[@nilsoncorrea8474]

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

[@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).

[@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??

[@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.