Epinefrine / Adrenalin in Cardiac Arrest Management

This podcast talks about quite a few different studies on Cardiac arrest, including a good double-blind, placebo controlled study on EMS use of Epi in Australia.

It's a lengthy podcast, and the guy is a bit annoying, but I enjoyed it. Further to that is the more recent Japanese study, Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest

The research is showing that the drugs we give are increasing the likelihood of a return of circulation, but show no significant increase in survival to discharge. Is the routine use of Epi etc bringing pulses back in patients that have no realistic chance of survival with intact neurological function?

I'm interested to hear what the Arrse / RAMC brain trust has to say on this. Currently I'm out in California and my agency's cardiac arrest protocols can be found here. We have a comparable survival rate to other 911 agencies in the US but having never worked in the UK I'm interested to hear the NHS view of all this. Especially in the prehospital environment.
I would expect adrenaline, through its vasopressor effects and its ability to increase cardiac output to improve outcome in cardiac arrest. However its effects are short-lived and I wouldn't expect it to have any effect on survivial to discharge and beyond. Long term survival rates after cardiac arrest could only be influenced by tackling the underlying cause of the arrest (assuming the condition is treatable and many are not). If the study has sufficient numbers some sub-group analysis would be useful, i.e. remove all those whose cardiac arrest was due to a long term and largely untreatable conditions (e.g. COPD, IHD etc) and then examine survival rates in the remainder, it might well show such patients had better survival rates. It would be interesting to hear how the investigators managed to get ethical approval for a placebo controlled study. How do you enroll a research subject into the study with informed consent when they are in cardiac arrest? What about those patients (now dead) who may have survived if they'd been given adrenaline but got saline instead?
I haven't read the entire Japanese study, but they don't / didn't routinely use Epi in cardiac arrest in Australia. So instead they just had to just get permission to do an Epi trial. However, even though they weren't using it anyway, politics got involved and people started getting worried about not using Epi all of a sudden... They still managed to analyze around 500 cases, but they were hoping for something closer to 5,000.

The drugs vs no drugs results didn't show any statistically significant difference in over all survival rates, only an increase in ROSC.

There is a retrospective study that analyzes the underlining causes but I can't find it. IIRC drowning had a pretty good survival rate, but they couldn't definitely say if it was due to the mechanism or because of any hypothermia / mammalian dive reflex stuff.
Yes, there is no hardevidence to show adrenaline makes a difference to survival yet ILCOR are reluctant to remove it from the guidelines because the known benefits MAY help.
Some interesting stuff has ben shown on the use of vasopressin but again, a reluctance to introduce in to the guideline.
In the UK we throw away £100,000s of out of date, unused adrenaline prefilled devices on the back of poor, or no evidence to support it's continued use in the management of cardiac arrest.
I'm hopeful that some real debate will come about because of the Japanese study. It feels to me like the standard use of high dose epi is just creating organ donors, and getting pulses back in PT's who have no realistic capability of making a recovery.

Vasopressin is interesting. It's in my scope but my agency doesn't stock it. I've heard stories of it turning peoples' fingers and toes black!
As far as I was aware, the best thing to do is maintain good chest compression's (ideally with a defib as well)... Adrenaline was just there as a bit on the side...
The organ donor point is a good one, have any studies been done on this?
From experience, adrenaline actually has very little effect other than a transient one in cardiac arrest. Like all the drugs used, other than oxygen, there is no real proven benefit for any of them. Again, from experience as a Resuscitation Officer, I would say that if the victim is at the stage where they are requiring any drugs, the outcome is generally going to be poor.

Just a few stats from "a hospital somewhere in England" during 2011. Of the 116 cardiac arrests only 16 did not have adrenaline. 24 survived to discharge, all 16 of those who did not need adrenaline being among that number. 23 of those "survivors" had their cardiac arrest pre-hospital, in A&E, in CCU, in the catheter lab or in ITU.

Three have since died, two of whom were pre-hospital events, and all three having required adrenaline at the time of their arrest.
...all 16 of those who did not need adrenaline...
Which suggests they were shockable (VF/VT) or PEA that was swiftly resolved before the team got there.
Hardly surprising they survived!
Your ALS manual will also be packed with interesting facts and figures, do feel free to share
Adrenaline in cardiac failure has been shown to be detrimental to outcome. In my experience in a large regional cardiac center with referrals from DGHs for patients with cardiac failure, these patients have been given large doses of Adrenaline by infusion. Recently I saw one on 4mg in 50mls at 22mls an hour plus Nor-adrenaline 4mg in 50 mls at 22mls an hour and also Dobutamine 250mg in 50mls at 6mls an hour. We immediately started Milrinone 10mg in 50 mls at 5mls an hour. Within 2 hours we had stopped the Adrenaline by the use of Milrinone. This level of drug therapy increases both preload and afterload in patients who are frequently hypovolaemic due to initial treatment modalities of diuresis and vasodilataion. Transthroacic or even better transoesphageal echocardiography is very useful for management also the use of a pulmonary artery catheter to assess vascular resistance and cardiac output. Mechanical support of at least an intra-aortic balloon pump in my opinion should be mandatory.

Adrenaline can be highly arrhythmogenic and increases myocardial oxygen (MvO2) demand by increasing workload, in the presence of a poor coronary circulation. Cardiac failure maybe exacerbated by Adrenaline by increasing afterload.

Adrenaline is not routinely used in cardiac surgical patients post op, because of the attendant risk of valve or graft failure unless prescribed by a senior member of the medical staff. In this case if resuscitation is not immediately successful by defibrillation, pacing or reversal of the 4Hs and 4Ts, immediate chest opening is mandatory

Resuscitation in cardiac failure patients is frequently a fruitless exercise.
It's not scientific but every single one of my successful pre hospital (cardiac) resuscitations that went on to walk out of hospital weren't down long enough to get adrenaline.
It's not scientific but every single one of my successful pre hospital (cardiac) resuscitations that went on to walk out of hospital weren't down long enough to get adrenaline.
The only successful resus attempts that I have had (pre-hospital) have been with the use of electricity. I've not personally had a 'survival to discharge neurologically intact' with any patient that has got far enough down the algorhythym to require adrenaline.
The only successful resus attempts that I have had (pre-hospital) have been with the use of electricity. I've not personally had a 'survival to discharge neurologically intact' with any patient that has got far enough down the algorhythym to require adrenaline.
Pretty much the same as me then, though I've had one or two asystolic chokers who responded well to getting me in to dynorod their upper airways with those nasty instruments the Anaesthetists keep insisting we can't use.
Time is of the essence as we all know, a hypoxic myocardium is so much more difficult to defibrillate, effective CPR does improve the patients chances. The outcomes no matter what we do are poor but saying that the underlying diagnosis is so important to success. For instance a 70 yr old with heart failure is generally unrecoverable, but as in the Fabrice Muamba case, effective sustained CPR using all the techniques available can be very successful.

Another form of resuscitation is ECCPR, as demonstrated in a Korean study, that percutaneous ECMO using Femoral arterial and venous cannulation, allows excellent oxygenation and Co2 removal is not dependent on any cardiac action. Unfortunately this is really only available for a very small patient group, acute MI in the catheter lab, hypothermia or even drug overdose, in a large cardiac centre. This was demonstrated by a case in Norway using cardio pulmonary bypass to resuscitate a doctor who when skiing fell brought some ice in a river, was flushed continuously with cold water until she fibrillated, she was then released, continuous CPR until she was on bypass and slowly warmed. She survived with tingling in her hands which stopped her career choice of eing a surgeon.

But getting back to the topic, no doubt the case for adrenaline when the guidelines are again reviewed, will up for much discussion. It s a nasty horrible drug with too many effects that may actually hinder cardiac action by increasing afterload.
It's not scientific but every single one of my successful pre hospital (cardiac) resuscitations that went on to walk out of hospital weren't down long enough to get adrenaline.
I'd be careful here, the plural of anecdote isn't data...

I'm in an uncomfortable position here in California. I've seen MANY studies that show Epi to be harmful, yet my protocols say I have to use it. One minute of drug free CPR, rhythm check, shock / no-shock, resume CPR and push 1mg of Epi, and another one 4mins later... I feel like Dr Frankenstein, I'm re-animating corpses.

Out of curiosity, does anyone have an experience with Levofed (Nor-Epi) and Vasopressin? Levofed is no longer in our protocols here but Vasopressin is as an Epi substitute.

And to further compound the whole cardiac arrest problem, a study done out here on dead piggies shows that supraglotic airways (combitube, King Tube, LMA) put pressure on the carotids and actually decreased cerebral perfusion... Add this to the existing study (that I can't find) that shows BVM gives better neurological outcomes than intubation, is there going to be much left for us to do?!

I'm not actually worried about running out of things to do, I just wonder what my colleges and other providers think about this stuff. Personally, I don't like to intubate until we get ROSC unless it's cardiac arrest secondary to hypoxia / respiratory arrest.
The problem with Vasopressin is that it is very responsive in a very small dose and I suspect that the increase in afterload may increase the risks of severe left heart failure by reducing stroke volume with the increase in vasoconstriction. Its also can kill of a liver very very quickly as I've seen happen in the past when used as an infusion.

Intubation in some patients in particular those with cervical spondylosis is normally fraught with hazard in particular fragmentation of carotid plaque and an LMA is also able to obstruct the carotids.
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