I'm aware of adrenaline's various problematic side effects, and its a doosey of a pickle. None the less, it does seem to improve ROSC, and perhaps if it were administered more often during the circulatory phase of an arrest rather than at ~19 mins like it normally is, you might see some improvement.
Are you suggesting escalating doses of epi, or more frequent doses? I'm not sure why you would wait 19 minutes to administer epi, that certainly doesn't fit any consensus that I've seen. Maybe I am misunderstanding what you are saying?
Behringer and colleagues studied the cumulative dose of api in cardiac arrest and found that higher doses are associated with worse neurological outcomes, even after adjusting for length of resus attempt. There have also been studies into high-dose epi, escalating dose epi, epi and vasopression, and epi or vasopressin. None have shown any benefit so I'm not convinced that more frequent or larger doses is the way to go.
I don't doubt that there is going to be a better drug than adrenaline for achieving a ROSC, but right now if the hospitals improve their management process, and the admission-to-discharge-without-deficit ratio, then achieving ROSC becomes more important. So long as adrenaline doesn't negatively effect survival to discharge, and it continues to improve ROSC, once you improve the ED process, adrenaline becomes a link in the chain that improves outcomes.
Hospitals have indeed been improving their management of post-arrest patients, and I have no doubt that they will continue to try to do so. However one of the great frustrations of cardiac arrest statistics is that in spite of ongoing, incremental improvements in hospital management of post-arrest patients, outcomes from arrest have remained essentially static for decades. This has been commented on frequently in the research.
To expect that all the woes of the post-arrest patient can be managed by the hospital is to abrogate all responsibility towards improved pre-hospital management and research. We may as well just do CPR until we get to hospital (which seems to be the case in many places anyway)
The bulk of the research going on today is pointing towards the management of the arrest with ACLS being of little value, but the management of post-arrest syndrome as being of paramount importance.
CCR is a good example of this. An emphasis on the basics but an acknowledgment that early adrenaline in the circulatory phase improves ROSC. You then couple this with agressive ED and ICU management and you have yourself your improved survival to discharge.
Except that you don't. ROSC is important, but to only consider ROSC as the endpoint that EMS needs to be aiming for is to provide substandard care for our patients. For example, if I were to develop a drug, lets call it Resusciton, that improved the rates of ROSC from cardiac arrest by 4 times when compared to epi, we would all be excited. However, if it were found then that patients treated with resusciton had a survival to discharge rate of 0.002%, then it quite rightly would be discarded. This may be the situation that faces us with epi: we may be increasing ROSC, but we may not be increasing discharge rates
despite aggressive ER and ICU management that already takes place.
I think similar things could be said about amiodarone. I was considering this analogy and forgive me if its very flawed (its obviously a little flawed in the prognosis of disease processes but humour me), I never payed much attention in research methods classes in first year and I'm kicking myself for it now. Take a hypothetical sample of open fractures to ribs also causing tension pnemothorax. You introduce chest decompression and it improves survival to hospital admission because people aren't dying of hypoxia/reduced perfusion, but you then don't give them broad spectrum antibiotics for the open fracture. If you then see a ridiculously high fatality rate, lets say 96%, due to infection, it would be easy to obscure the value of the chest decompression in terms of survival-to-discharge without a sufficiently gigantic study?
It is entirely possible to adjust for a large number of variables in pre-hospital data (or any data for that matter) including things like in-hospital management. Sample size is important, and the larger the better, but there are many, many ways of extracting useful information from almost any set of data.
Post-ROSC hydrocortisone? Anyone doing it? I read an interesting paper yesterday on aggressive glucose control in acute coronary syndrome. Might we one day see similar for all inflammatory/ischaemia/poor perfusion conditions, me thinks. Control of glucose, control of excessive oxygen, therapeutic hypothermia, endocrine modulation, all in the prehospital environment.
Not yet. There is a lot more research that needs to be done before we necessarily start managing adrenal insufficiency post-arrest, but I suspect that sometime in the future we will be considering it.
[/QUOTE]Yes, simply remarking on the way in which "logic" in medicine can misdirect you. Its funny that you mention the topic though. One of my assignments this semester is to design a research study, methodologically and organizationally. We have to do everything except actually do it. I wanted to do something about supplemental oxygen in ACS or stroke (suggestions?). I'm quite fascinated by this idea that oxygen can do more harm than good and quite frustrated by the continued ubiquitous use of 8litres through a hudson for bucket loads of inappropriate patients. I've read the paper you mention and I think that the only relevance it really has to the prehospital field is that it seeds the idea in people who weren't previously aware of it.[/QUOTE]
I would hope that seeing how KIlgannon and friends are building on work that has been around for quite some time (ILCOR published recommendations for FiO2 in 2008, drawing on data from well before then) that people would have some idea of the dangers of hyperoxia. Maybe that is expecting to much.
I do, however think it is entirely relevant as typically it is EMS who starts resus with 100% O2 and continues the post-arrest management with the same, thereby potentially having a huge impact on oxidative stress in the early phases of reperfusion. It should certainly be enough for people to start questioning their management even if Medical Directors are not yet changing protocols based off this (and other) research.
) and this study didn't start measurements until 24 hours post arrest. However I suspect that this might be another area where some significant research could be carried out in the field. Well, maybe not in the States, but hopefully in Europe or the Antipodes!
