Bernard's 2002 RCT didn't involve infusion of cold fluids.
Bernard's later trial (I think it began in 2006) Rapid Infusion of Cold Hartmans was inconclusive which is not surprising given the large number of participants you would need to show a statistical differences between starting a process that works over days, a few minutes earlier or later.
Yes it was his later study that I was thinking of (Induction of Therapeutic Hypothermia by Paramedics After Resuscitation From Out-of-Hospital Ventricular Fibrillation Cardiac Arrest. A Randomized Controlled Trial, Circulation 2010), although there have been a number of small studies published by other authors as well (some from Sweden if I'm not mistaken)
I think the key to further investigation in this field, given Bernards results is indeed about the minutes as opposed to hours or days. If we can preemptively manage reperfusion injury by starting cooling during the arrest rather than after it, it would seem logical that this would be of benefit. Of course logic and medicine don't always go together that well!
No. I only heard about two weeks ago and I couldn't find it in the clinical trials registry. I'm ganna try and find out more about it this week.
I found the trial at
http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01172678 which is the National Institutes of Health clinical trial website. I don't know if or where it is published elsewhere.
I don't buy that ACLS is not beneficial or harmful. I think you just need to remember your priorities. If paramedics are too stupid to remember that compressions mean more than IV access, that's not the fault of the ACLS drugs. Also I don't think that its the responsibility of the ACLS drugs to secure a survival to discharge, I think that becomes the responsibility of aggressive ED and ICU management, cath labs for all arrests regardless of conscious state, universal acceptance of cooling. I think ED management needs to be much more protocolised...a la...surviving sepsis guidelines. I'm sure they've got it covered at the big teaching hospitals, but I've been to plenty of smaller hospitals where I rather stick with the MICA paramedics than be turned over to some scarred bunch of registrars if I'd arrested
I have to disagree. There is ample evidence that, whilst ACLS drugs may increase the likelihood of ROSC, that does not translate into survival to discharge. There is also a large body of evidence that our mainstay of ACLS, epinepherine, is associated with worse outcomes, probably from O2 supply/demand mismatch, myocardial dysfunction, pulmonary shunting and neurological dysfunction. These effects are independant of the quality of CPR: it is the drugs that are the cuplrits. I also think that survival to discharge is the only real measurement we should be interested in. We can get a huge percentage of people to hospital with a pulse, but this means nothing if they are not discharged at all, or discharged with gross neurological defecits. This was highlighted in some ways by the ARREST trial that brought amiodarone sweeping in to our drug boxes. An exciting difference of 24% versus 12% survival to hospital was seen in the amiodarone versus lidocaine groups. However an utterly non-significant 6% versus 5% was seen in survival to discharge.
One must presume that overall the ED management of these two groups was similar, and that the (lack of) difference is therefore attributed to the pharmacology being tested. To assume otherwise would essentially eliminate any possibility of carrying out pre-hospital research as any difference (or lack of) can be attributed to the hospital and the management the patient recieves there.
In Bernards first trial however, patients were only enrolled if they were being taken to a small number of selected hospitals, presumably to allow for a standardized level of care in the ER and ICU.
This is not to say that differences in the level of care in hospital won't have an impact on outcomes, and this is indeed why there are calls for post-arrest care bundles such as those put forward for sepsis patients. However this cannot negate the need for ambulance services and medical directors to carry out high quality research into our impact on survival to discharge.
Re pressors/inotropes: what do you use/how do you titrate/to what do you titrate? From my reading the popular combination seems to dobutamine and noradrenaline in hospital as long as the CVP and Hb are squits. Although I've also glossed over some papers that showed little difference between the combination and between dopamine and adrenaline...so whats the deal?
Broadly speaking, the choice of inotrope probably doesn't matter. There is no compelling evidence for any particular inotrope in managing BP, so selection will essentially come down to what your medical director prefers. That said, there is evidence that epinepherine during cardiac arrest is associated with post-arrest myocardial and neurological dysfunction, although obviously this is given in much higher concentrations than one would expect to see with an infusion to maintain perfusion.
Interestingly enough, post cardiac arrest adrenal insufficiency may be a relatively common syndrome in those patients in whom it is difficult to maintain blood pressure. Where else do we see this? Sepsis! That pesky old duo SIRS and CARS at it again!
While Hochman (amongst others) has demonstrated that inotropes in heart failure do not improve outcome (that old supply/demand thing again) it is apparent that in most cases of poor cardiac index post-resus, the culprit is more likely to be global myocardial stunning, such as that seen in sepsis, which is of course reversible so long as perfusion is maintained for the first 24 hours or so.
Ultimately I guess, it probably doesn't matter too much: they all end up as epi anyway! Use what you've got until some more compelling evidence arrives one way or another.
