# Post cardiac arrest management.



## Smash (Aug 12, 2010)

Hello.

I'm curious about post cardiac arrest managment.  How does everyone go about managing the post return of spontaneous circulation (ROSC) patient prior to and during transport to hospital?

Namely:  

-How do you manage time/transport?  Do you throw the patient straight on the gurney as soon as you get ROSC, or do you attempt to manage any problems prior to moving?

-What blood pressure do you accept as being adequate?  

-If you manage blood pressure actively, how do you do so?  

-How do you manage airway and ventilation/oxygenation?  

-Do you use therapeutic hypothermia, and if so, by what method?

and finally, if you know it, what are your survival to discharge rates for patients presenting in VT/VF?

Thanks for your time.


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## 8jimi8 (Aug 12, 2010)

never worked an ooh arrest.  All of my experience is in the ER or the ICU and never had anyone that didn't immediately code over and over.  It's sad when you code a guy so many times that the ER doc stops coming to help.  Never got to induce hypothermia on anyone, only watched one for 3 hours before my shift was up.

Althought i did get to push mag on a guy once... he was stable for about 10 minutes after that.

was truly an awesome experience getting to be a new grad on the code blue team.

all ears from this point on.

...vt/vf survival rates i saw were 0%


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## 94H (Aug 12, 2010)

For the only code that I had spontaneous circulation return to we needed to send a copy of the rythm to the Med Director so he could make a decision on which facility to transport to. 

The first blood pressure we took once we realized that circulation had returned was the one we used (It was pretty decent though so we didnt need to manage it at all)

We kept baggin the pt since they didnt have return of respirations

No idea about survival, all i know is we were still bagging when we got to the ER and handed em off


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## MasterIntubator (Aug 12, 2010)

Smash said:


> Hello.
> 
> I'm curious about post cardiac arrest managment.  How does everyone go about managing the post return of spontaneous circulation (ROSC) patient prior to and during transport to hospital?
> 
> ...



Be patient.... your rewards will come.


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## Aidey (Aug 12, 2010)

Smash said:


> Hello.
> 
> I'm curious about post cardiac arrest managment.  How does everyone go about managing the post return of spontaneous circulation (ROSC) patient prior to and during transport to hospital?
> 
> ...




1. Depends on what the problems are, but usually yes. If we get ROSC we then will c-collar and back board the patient. The c-collar is to keep the neck midline to help prevent the tube from being dislodged, and the board is in case  they code again. If they still have a pulse after all of that then we transport. If they don't, we go back to working the code right there. 

2. Fluids or dopamine. If the pt is bradycardic we will give atropine for that and see if the BP comes up before doing anything else.

3. Reassess the tube and make sure it is still good. That means lung sounds, chest rise, ETCO2 - both number and waveform. 

4. Nope, not yet. 

5. 0. All of my ROSC patients have been in PEA or asystole (2, and yes it really was asystole). The longest surviving patient was a witnessed arrest, we did one whole round of CPR and gave an Epi and he came back. He died 3 days later in the ICU from septic pneumonia (in 4 of 5 lobes), rhabdomyalosis with acute kidney failure and severe liver dysfunction. Don't ask me how he made it 3 days.


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## Smash (Aug 13, 2010)

MasterIntubator said:
			
		

> I am happy with anything above 80 systolic. We can work with that, and if it holds over 80, I am assured that the vital end organs are getting perfused






Aidey said:


> 2. Fluids or dopamine. If the pt is bradycardic we will give atropine for that and see if the BP comes up before doing anything else.



What BP (or MAP) do you aim for?  I'm particularly interested in management of post-resuscitation syndrome and mitigating reperfusion injury and derangements of cerebral blood flow that come with anoxic brain injury.  There is a plenty of evidence that supranormal MAP post-resuscitation is important in maintaining cerbral perfusion in the face of loss of autoregulation and cerebral hypoperfusion post arrest.  Elevating BP, hemodilution and hypothermia are all critical to successful outcomes post cardiac arrest, so I find it interesting that a BP of 80 systolic is considered adequate.

I'm also interested in the uptake (or lack of) therapeutic hypothermia post arrest.  What is it that stops agencies from adding this to their protocols?


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## MasterIntubator (Aug 13, 2010)

Ahhhh.... your college level question excites me... 

MAPs.... the under-taught secret world of BPs.  Why don't they teach more about that and the significance?  I dunno.  Maybe its a higher learning, maybe its mis-understood.

Seriously though....  I *aim* a BP somehere normal enough to give me a MAP of 80.  In my dream world.... I would just get CPP enroute to the hospital to maintain 15 or so, but we don't have the transcranial dopplers for that in field.  But I will settle for 80 systiolic for a short time. Can't rush it, let the body work to catch up, then intervene

I figure in my short trip once enroute to the ED ( 5-10 min ), if I can maintain CPP at a minimum or better, then a systolic of 80 will suit me fine, as I will have my hands full and will be quite busy using my time efficiently. 

Of course, if I find myself on some mutual aid call, and my enroute time to the ED is 30-45 minutes, I will most likely have more time to change my stratagy. I will have more time to see the results and wait for drugs to kick in while the body tries to regulate itself.

My rationalle... if I need a systolic pressure of 60-70mmHg to maintain cerebral perfusion, a systolic of 80 or better will get me there factoring in any cardiovascular resistance that may hinder my efforts.  Also, there are many tools that I lack in the field that would be available in the hospital setting... like chems.  The chems will most likely be out of whack, and in order to assist the reperfusion process, you need them chems ( esp the electrolytes ) in the normal ranges. 

Yes, higher MAPs and CPPs are have shown to have a better outcome and lessen the chance of reperfusion injury.  Just as mild hypothermia.  

We know mild hypothermia is most likely beneficial, but what time frame do we have?  We know the first 24 hours are key.... but do you have some buffer time to get that rolling?  Like an hour?   Remains to be seen.
Metoprolol hit that road a couple years ago.  Yes, Betas are benificial... but we have a window to give it.  Let the cardiac insult stabilize, then give it. 

Most all of my ROSC cases came back normotensive to hypertensive.  Possibly because all those pressors and stimulants we gave during the code are reaching full potential.  So, hypotension has not been a big deal initially right after a ROSC for us if given a little time to let the body regulate and reperfuse.  ( a little time is defined as 5-10 minutes... which = almost at the ED ).  I use that time to check the basics, BG, airway, etc. 

Those are just my views from past experiences, and it has been working well for the past 5 years.  Not sure what else to tell ya.  
Maybe in 5 more years, I will find out that posterior chest compressions with the head in an ice bath works better.


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## Melclin (Aug 13, 2010)

Smash said:


> -How do you manage time/transport? Do you throw the patient straight on the gurney as soon as you get ROSC, or do you attempt to manage any problems prior to moving?
> 
> -What blood pressure do you accept as being adequate?
> 
> ...



Blood pressure is managed post-resuscitation with adrenaline boluses until an infusion can be setup. When we talk about pressure management post-ROSC we talk about a MAP of 70-90. Its more the realm of the MICA paramedic, and I've read a few PCRs that show them tapering the infusion at around 90. 

Fluids obviously have a roll to play if we believe they are volume depleted.

Airway wise, at the Ambulance Paramedic level, its LMAs and I believe they are underutilized in our service. Manual ventilations and if we're out in the country we might have etCO2 to guide us. MICA always have etCO2 and intubation via whatever method is appropriate depending on the GCS of the person. RSI in continued coma and not already tubed.

Therapeutic hypothermia is the go via the rapid infusion of 2L of cold normal saline. I've heard on the grape vine that Stephen Bernard's RCT on Rapid Infusion of Cold Hartmanns (RICH) trial failed to show an improvement in outcomes, which is a bit disappointing. 

This study is survey of reasons why American EMS systems are not using therapeutic hypothermia:

Suffoletto BP, Salcido DD, Menegazzi JJ, National Association of Emergency Medical Services P. Use of prehospital-induced hypothermia after out-of-hospital cardiac arrest: a survey of the National Association of Emergency Medical Services Physicians. Prehosp Emerg Care. 2008 Jan-Mar;12(1):52-6.

Anyone using dobutamine/noradrenaline? 

Seems a bit of a long shot on account of not being able to monitor CVP but is anyone treating hypertension with NTG?


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## MasterIntubator (Aug 13, 2010)

NTG for HTN... not any more.  At least not without the presence of CHF/Pulm edema, STEMI or something else outwieghing the risks of CVA or ischemia by treating HTN alone.  In the 90s we used to use Procardia for HTN... but that was halted on asymptomatic HTN.


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## Smash (Aug 14, 2010)

So what about all the lurkers?  Or does no-one else manage post arrest patients? <_<


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## MrBrown (Aug 14, 2010)

We do not have a blood pressure range nor any formal guidance on this area.

Airway control at Paramedic level is by use of the LMA which by all accounts works well.  Intensive Care Paramedics have intubation and some have RSI.  

Therapuetic hypothermia is not being used here as there is (in the eyes of the CMG) no evidence that the benefit of in-hospital cooling extends to the pre-hospital environment.  Post arrest patients are however not to be covered nor any attempt made to warm them.


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## Smash (Aug 15, 2010)

MrBrown said:


> We do not have a blood pressure range nor any formal guidance on this area.



If not in protocol, is there a generally accepted acceptable blood pressure for the medics in the field?  If so (or not) what is this based on?



> Therapuetic hypothermia is not being used here as there is (in the eyes of the CMG) no evidence that the benefit of in-hospital cooling extends to the pre-hospital environment.  Post arrest patients are however not to be covered nor any attempt made to warm them.



That is fair comment, the evidence as to the timing of hypotermia is particularly scarce.  However, to my mind it would seem logical that earlier = better.  What we are trying to minimize is essentially reperfusion injury.  That injury begins occuring at the moment of reperfusion (ROSC) and continues in different phases from then.  It would seem logical then, that the sooner we start to manage that, the better.  Hopefully we will see some data out in the next couple of years that may support or refute that position


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## MrBrown (Aug 15, 2010)

The problem with the scientific method and EBM is that absense of evidence is often seen to indicate evidence of absense where logical thought is disregarded because some data does not exist to back it up.


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## Melclin (Aug 15, 2010)

Smash said:


> If not in protocol, is there a generally accepted acceptable blood pressure for the medics in the field?  If so (or not) what is this based on?
> 
> 
> 
> That is fair comment, the evidence as to the timing of hypotermia is particularly scarce.  However, to my mind it would seem logical that earlier = better.



Appologies if I'm telling you things you already know, but I believe our service has recently begun a trial of cooling during cardiac arrest and continuing after ROSC in the standard way. Do you know anything more about that sort of idea?

A couple of animal studies show a correlation between earlier cooling and better outcomes if I remember correctly, which i assume is what you mean by scarce. Although, I think, of the two RCTs that support hypothermia, bernard's one involved prehospital cooling with ice packs didn't it? So while rapid infusion of cold saline is not _exactly_ supported, in a sense prehospital cooling is. To my mind, that and the fact that it makes sense intuitively/physiologically is enough to keep going at least until some conclusive proof that its useless. 

Apparently, half the reason we kept on with it after the RICH trial didn't come back positively, was to remind hospitals to continue it.


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## Smash (Aug 15, 2010)

Melclin said:


> Appologies if I'm telling you things you already know, but I believe our service has recently begun a trial of cooling during cardiac arrest and continuing after ROSC in the standard way. Do you know anything more about that sort of idea?
> 
> A couple of animal studies show a correlation between earlier cooling and better outcomes if I remember correctly, which i assume is what you mean by scarce. Although, I think, of the two RCTs that support hypothermia, bernard's one involved prehospital cooling with ice packs didn't it? So while rapid infusion of cold saline is not _exactly_ supported, in a sense prehospital cooling is. To my mind, that and the fact that it makes sense intuitively/physiologically is enough to keep going at least until some conclusive proof that its useless.



Bernards trial was the one involving rapid infusion of cold crystalloids.  Whilst it didn't show any benefit as compared to in-hospital cooling, it did at elast demonstrate that the rapid bolus of cold fluid is a safe and effective means of reducing core temperature quickly.  What remains to be seen is whether instituting this earlier is of any benefit (ie. during the arrest as discussed above) which seems to be what your service is attempting.

Of the methods of cooling, the one that intuitively makes most sense to me is the cold fluid.  Induced hypothermia is the standard of care now (notwithstanding some gaps in the knowledge), and hypertension is also relatively well studied (well, relatively) but there is also some reasonably compelling evidence that hemodilution improves cerebral blood flow both in animal models of cardiac arrest, some small human series and also extrapolated from other studies such as in stroke.
Therefore, to my way of thinking, cold fluid attacks all the issues of hypothermia, hemodilution and to some extent, hypertension in one go.  We know that cold fluid doesn't impair cardiac function significantly post arrest, whereas inotropes (particularly epinepherine) do.  Therefore if we can take steps to maximise BP and cerebral blood flow whilst minimizing reliance on drugs, all the better it would seem (warning, last sentence was opinion, not evidence...)

Do you know when your trial of hypothermia during arrest is anticipated to end?

I'm somewhat bemused by the lack of interest in this.  We know that ALS _during_ cardiac arrest is quite possibly not beneficial and probably even harmful, yet there is compelling evidence that post-arrest management is of the utmost importance in ensuring that those who do respond to CPR and defib have a chance at returning to some kind of functionality.  If ALS providers aren't interested in post-arrest management, what _are_ they interested in?! :blink:


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## Melclin (Aug 16, 2010)

*Wait..which of Bernard's....*



Smash said:


> Bernards trial was the one involving rapid infusion of cold crystalloids.  Whilst it didn't show any benefit as compared to in-hospital cooling, it did at elast demonstrate that the rapid bolus of cold fluid is a safe and effective means of reducing core temperature quickly.  What remains to be seen is whether instituting this earlier is of any benefit (ie. during the arrest as discussed above) which seems to be what your service is attempting.



Bernard's 2002 RCT didn't involve infusion of cold fluids. It involved aggressive use of ice packs around the head and groin. This process was started in the prehospital environment. (MICA paramedics are fond of telling anecdotes about stopping at gas stations to pick up bags of ice for post-ROSC pts.) This is one of two proper RCTs that supports the use of cooling, although neither involve rapid infusion of cold crystaloid. So there is evidence that supports cooling from ROSC by paramedics, just not that it makes any difference whether or not it is started in the prehospital environment or if you can wait untill hospital. That fact that one of the major RCTs that supports cooling in hospital necessarily involved prehospital cooling, makes it a done deal in my opinion. 

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.   




> Therefore, to my way of thinking, cold fluid attacks all the issues of hypothermia, hemodilution and to some extent, hypertension in one go.



I completely agree and I especially like the idea of haemodilution. Its a mystery to me why there hasn't been more research into haemodiluting cardiac arrest patients, it makes pretty good sense to me.



> Do you know when your trial of hypothermia during arrest is anticipated to end?



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'm somewhat bemused by the lack of interest in this.  We know that ALS _during_ cardiac arrest is quite possibly not beneficial and probably even harmful, yet there is compelling evidence that post-arrest management is of the utmost importance in ensuring that those who do respond to CPR and defib have a chance at returning to some kind of functionality.  If ALS providers aren't interested in post-arrest management, what _are_ they interested in?! :blink:



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 

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?


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## Smash (Aug 16, 2010)

Melclin said:


> 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.


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## Melclin (Aug 16, 2010)

Smash said:


> 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),



Didn't know it had been published. Having a good read of it now. I notice that the difference in temp between groups was 0.8 degrees, for well, looks like about ~1 hour. Which is what I was getting at when I said it was not surprising that the trial didn't show a positive result on account of sample size. They also mention that in the discussion.


My word you're johnny on the spot with the journals. Don't happen to know if he's published the RSI findings properly yet do you? Its well past time for it, so I figure its out and missed it. I've seen the results presented by bernard and I've seen abstracts but no formal publication as yet.



> 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 they certainly don't. I agree with you about the logic of earlier = better but it just all depends on much better understanding of the physiology of arrest and post-ROSC pts. Resus will be an interesting place to be in the next 20 years. Oxygen is good right? We need it to live, so it must be life giving. If sick, give more oxygen. So just turn the flow meter up yeah? 





> 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.



Yep RINSE is the name. I reckon they might be pushing it to get 1300 in 3 years. 

I haven't the time to write back about the ACLS drugs right now, gotta write an essay on hospital bypass...:wacko: ...I'll be back.


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## Smash (Aug 16, 2010)

Melclin said:


> My word you're johnny on the spot with the journals. Don't happen to know if he's published the RSI findings properly yet do you? Its well past time for it, so I figure its out and missed it. I've seen the results presented by bernard and I've seen abstracts but no formal publication as yet.



No, I haven't seen it anywhere yet, which is quite disappointing.  My understanding from what I have seen presented and discussed, is that it a very high quality study in terms of methodolgy (most RSI trials have merely shown that a procedure done badly is bad for the patient), and shows a clear benefit in a certain subset of patients with TBI.  However I think that there was a trend towards more cardiac arrests in the RSI arm, so perhaps they are mining this data further before publishing?  I don't know whether the trend was significant (statistically speaking) or not.



> No they certainly don't. I agree with you about the logic of earlier = better but it just all depends on much better understanding of the physiology of arrest and post-ROSC pts. Resus will be an interesting place to be in the next 20 years. Oxygen is good right? We need it to live, so it must be life giving. If sick, give more oxygen. So just turn the flow meter up yeah?



LOL, you would think that to be that case, certainly if the medic mills are to be believed, but I beg to differ.... Kilgannon JH, Jones AE, Shapiro NI; et al, Emergency Medicine Shock Research Network (EMShockNet) Investigators. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010;303(21):2165-2171

Apparently oxygen reactive species aren't just something for the vitamin shysters to use to push their products on us anymore! 

There are some significant limitations to this study, particularly as there is evidence that early hyperoxia is more harmful than late, due to that first rush of oxidative damage upon reperfusion (how could we limit that I wonder  ) 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!



> Yep RINSE is the name. I reckon they might be pushing it to get 1300 in 3 years.
> 
> I haven't the time to write back about the ACLS drugs right now, gotta write an essay on hospital bypass...:wacko: ...I'll be back.



Looking at the exclusion criteria, that would certainly rule out most cardiac arrests where I work!  

Resus (and post-resus) certainly is a fascinating area of research that has potential to have wide-sweeping changes to paramedic practice the world over.  This is part of the reason I find it fascinating that there are very few people on the forums who appear interested in it...


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## MrBrown (Aug 16, 2010)

Smash said:


> Resus (and post-resus) certainly is a fascinating area of research that has potential to have wide-sweeping changes to paramedic practice the world over.  This is part of the reason I find it fascinating that there are very few people on the forums who appear interested in it...



Hey! Brown was at the store having his jumpsuit custom fitted and paid for.

They wouldn't sell me a large reflectorised slip-in label for the back that said "DOCTOR" however.  Oh well, I suppose I have to earn that.  

From my fleeting musings and glances it would appear much work is being done on reperfusion injury and the effects of oxygen on tissues and organs.  Highly fascinating.

And yes, oxygen can be bad.  Trust me, I know.


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## Smash (Aug 18, 2010)

*Really?*

So no other ALS providers manage post arrest patients?  I do find that strange.  Maybe you all just do CPR to hospital?


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## Melclin (Aug 19, 2010)

Smash said:


> 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.



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. 

If we think of an arrest patient as having a two part problem, the first being the arrest itself and second being the post resuscitation syndrome, then its unfair to expect a drug that works on the arrest to improve the other if the other is pervasive enough to obscure the survival effects of the previous, in all but the largest of trials. 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. 

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.   

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? 




> 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!



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. 



Smash said:


> LOL, you would think that to be that case, certainly if the medic mills are to be believed, but I beg to differ.... Kilgannon JH, Jones AE, Shapiro NI; et al, Emergency Medicine Shock Research Network (EMShockNet) Investigators. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010;303(21):2165-2171
> 
> Apparently oxygen reactive species aren't just something for the vitamin shysters to use to push their products on us anymore!
> 
> There are some significant limitations to this study, particularly as there is evidence that early hyperoxia is more harmful than late, due to that first rush of oxidative damage upon reperfusion (how could we limit that I wonder  ) 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!



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.


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## Smash (Aug 21, 2010)

Melclin said:


> 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.


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## Smash (Aug 31, 2010)

Just thought I might give this a nudge to see I'd anyone has started caring for post-arrest patients yet... I'd love to hear from you if you have!


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## Melclin (Aug 31, 2010)

*Weird*

I'm quite sure I replied to your last post yonks ago. Frustrating.

In short, because I can't be arsed typing it all out again, it read something like:

Adrenaline: I didn't mean frequency or dosage escalation, I meant earlier administration..more often. There has been some suggestion of giving IO and carpujects of adrenaline to first responders on the basis that it may be useful at 4 or 5 mins after an arrest but at the standard 19 mins it takes for ALS to turn up and stick the pt, its useless. 

ACLS: Some confusion lays in the terminology. We don't use "ACLS - the algorithm", our arrest management is not as heavily protocolised (probably to our detriment in some cases). Our management is of course based on the same idea, but when you say ACLS, I just think loosely of the concepts and drugs involved, not strictly about a protocol. Its a descriptive term to me, not a propriety set of treatments which it seems to be in the US. For example, advanced post-ROSC care is what I'd consider to be advanced cardiac life support, but it seems its not ACLS...? I argue for ACLS because I think of that as including advanced _thought out_ care by people who can prioritize treatments, appropriately apply drugs during and after an arrest, RSI and cool a ROSC patient, etc.

Resuscitation: I get the idea of better ROSC but worse survival to discharge. But the same studies that show epi doesn't have a survival benefit all seem to also say that it doesn't reduce survival to discharge either. I'm not at all saying that we should ignore survival to discharge (they need an initialism for that..badly) as an outcome measure, of course ultimately its the most important part. But Im also saying that survival to admission shouldn't be ignored. Its at least an indicator of some kind of success and I think the intricacy of relationships between treatments needs more thought. I think its overly simplistic to say, epi = no survival benefit = not important. 

At the end of the day though, I do agree that its s**t hot compressions, early defib and good post-ROSC care that makes all the difference. I'm also disappointed although not overly surprised that more people haven't chimed in.


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## Smash (Aug 31, 2010)

Melclin said:


> I'm quite sure I replied to your last post yonks ago. Frustrating.
> 
> In short, because I can't be arsed typing it all out again, it read something like:
> 
> Adrenaline: I didn't mean frequency or dosage escalation, I meant earlier administration..more often. There has been some suggestion of giving IO and carpujects of adrenaline to first responders on the basis that it may be useful at 4 or 5 mins after an arrest but at the standard 19 mins it takes for ALS to turn up and stick the pt, its useless.



19 minutes?! :blink: Is that published, or a local thing?  To be fair I don't know the exact timing of when drugs are pushed here, but given that we (being ALS) are usually there around the 10 minute mark (on average -first response and BLIS/ILS sooner), I hope it is sooner!  
I see what you are saying about the earlier administration of epi though, it is an interesting idea.  I guess it would come down to how it is given and by whom.  Obviously it needs to be given IV, so we need to train first responders in some kind of venepuncture/IV skills.  We then run the risk (as often happens when people get new toys) of letting the good quality CPR and early defib fall by the wayside as providers fall prey to the technical imperative.




> Resuscitation: I get the idea of better ROSC but worse survival to discharge. But the same studies that show epi doesn't have a survival benefit all seem to also say that it doesn't reduce survival to discharge either. I'm not at all saying that we should ignore survival to discharge (they need an initialism for that..badly) as an outcome measure, of course ultimately its the most important part.


  Survival to discharge.. STD?  Maybe not...  I understand what you are saying about survival to hospital, but ultimately if we aren't getting them out of hospital we need to be reassessing how we go about our business.



> At the end of the day though, I do agree that its s**t hot compressions, early defib and good post-ROSC care that makes all the difference. I'm also disappointed although not overly surprised that more people haven't chimed in.



Maybe everyone just does CPR on corpses until they get to hospital, so they never have to manage post arrest patients?!


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## Melclin (Aug 31, 2010)

Yeah bit of a shock right? Rittenberger et al published it as an average time to administration for trials of ACLS drugs. The average time to admin in trials of drugs was 19.4 mins (I suppose you could be generous and add a minutes grace considering they have to crack and envelope and think about the trial for a bit). I mention this because Reynolds et al averaged the time to admin in the far more successful animal trials and it was significantly shorter (about 9 mins) and they postulated that the reason for their success was the shorter time to admin. I can't be arsed grabbing the paper now because I've gotta head off to uni, but I think they also mentioned that greater time to admin in the animal trials correlated with poor survival, whatever that's worth.


Rittenberger JC, Bost JM, Menegazzi JJ. Time to give the first medication during resuscitation in out-of-hospital cardiac arrest. Resuscitation. 2006;70:201—6

Reynolds JC, Rittenberger JC, Menegazzi JJ. Drug administration in animal studies of cardiac arrest does not reflect human clinical experience. Resuscitation. 2007;74(1):13-26.




> Survival to discharge.. STD? Maybe not... I understand what you are saying about survival to hospital, but ultimately if we aren't getting them out of hospital we need to be reassessing how we go about our business.



Lol. I definitely think that much more research needs to be done, and I do think ultimately we need a better alternative to adrenaline for all the negative physiological effects if not its poor showing in the RCTs. But I feel that's a given. Nobody would argue that we should sit on our hands 'cos we doin' the deaduns real awesome as it is'. But I just think that the results of these RCTs can overshadow the complexity of matter. I just don't like the "adrenaline, 1mg, 3minutely - yay or nay?" questions. I think we'd risk ignoring the intricacy of the issue and not answering further questions like, "will it work better if we give it earlier", "would it work better as an infusion", "would it work if we added drug x and oh look now things work better". Anyway I'm flogging a dead horse, you get my point.

I sure hope that we're past that idea. Although we're still transporting arrests in progress sometimes unfortunately. One of the problems with paramedics having a lot of autonomy I suppose. It relies on them being up to date, and if they're not...:unsure: (I shouldn't be unfair. There are a few reasons why that happens, mostly issues of resource allocation as far as I can tell).


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## Smash (Sep 1, 2010)

Thanks for the references, I'm not sure how I managed to overlook those in my travels.


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## Fox800 (Sep 1, 2010)

Smash said:


> Hello.
> 
> I'm curious about post cardiac arrest managment.  How does everyone go about managing the post return of spontaneous circulation (ROSC) patient prior to and during transport to hospital?
> 
> ...



Upon achieving ROSC, we immediately remove the ResQPod/ITD, take a manual blood pressure, and get a 12-lead. One paramedic does this with the first responders while the other paramedic gets things ready for transport. This involves hanging a bag of chilled saline and getting the backboard/stretcher ready for the patient. Our goal is to be off the scene in under 10 minutes after achieving ROSC.

We do have an invasive hypothermia protocol. However, the pt. must be over 18 years old, have an advanced airway in place, have an arrest from a presumed medical cause (trauma and hemorrhage are out), and have an SBP >100mmHg. If their pressure is under that, we give dopamine to raise it then we start cooling.

Airway maintenance is the same as it was before, minus the ResQPod. Patients will ideally have an endotracheal tube or King LT airway in place prior to ROSC.

Our hypothermia protocol consists of the following:
-Midazolam 5mg IV/IO titrate to effect with SBP >100
-Vecuronium 0.1mg IV/IO max dose 10mg
-Rapidly infuse 30mL/kg IV/IO COLD saline max 2 liters
-Can repeat vecuronium 0.01mg max dose 10mg if shivering/movement/awakening occurs (after administering additional midazolam of course)


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## Smash (Sep 4, 2010)

Fox800 said:


> Upon achieving ROSC, we immediately remove the ResQPod/ITD, take a manual blood pressure, and get a 12-lead. One paramedic does this with the first responders while the other paramedic gets things ready for transport. This involves hanging a bag of chilled saline and getting the backboard/stretcher ready for the patient. Our goal is to be off the scene in under 10 minutes after achieving ROSC.
> 
> We do have an invasive hypothermia protocol. However, the pt. must be over 18 years old, have an advanced airway in place, have an arrest from a presumed medical cause (trauma and hemorrhage are out), and have an SBP >100mmHg. If their pressure is under that, we give dopamine to raise it then we start cooling.
> 
> ...



Hi Fox800, thanks for your reply.  That care bundle is almost identical to ours, although we use different pharmacology to achieve the same goals.

Do you know your survival rates from VF/VT arrests?

How do you find the ITD?  I have no experience with them myself and haven't been able to find a lot of high quality data, but the idea seems sound.


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## EMTinNEPA (Sep 4, 2010)

Melclin said:


> Therapeutic hypothermia is the go via the rapid infusion of 2L of cold normal saline. I've heard on the grape vine that Stephen Bernard's RCT on Rapid Infusion of Cold Hartmanns (RICH) trial failed to show an improvement in outcomes, which is a bit disappointing.



The problem with therapeutic hypothermia is that it will stimulate the shivering reflex.  When the patient starts shivering, they'll be using up energy, which will just increase oxygen demand and serve no purpose whatsoever.  Therapeutic hypothermia has to be accompanied by a Neuromuscular Blocking Agent or heavy sedation to quell the shivering reflex in order to be effective.  I don't know about you, but the only sedatives I have are benzos... with a post-resuscitation, I would be cautious about anything that may effect the patient's blood pressure in a negative way.


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## EMTinNEPA (Sep 4, 2010)

To the OP...

1. Manage ABCs
2. Fluid or Dopamine to support blood pressure
3. If appropriate, a Lidocaine or Amiodarone drip
4. If bradycardiac, transcutaneous pacing
5. Treat any other issues that arise
6. Rapid diesel infusion


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## MasterIntubator (Sep 4, 2010)

EMTinNEPA said:


> 6. Rapid diesel infusion



I will have to politely disagree with #6.  This is where one should not run at high speeds to the ED.  Too many documented risks and crashes happen.  We should have the tools and the knowledge to manage while responding code at a safe speed.   ( and for those that already do, kudos too you! ).  Too many newer folks are not being taught valuable driving lessons in class prior to the road, and it shows out there.

Be safe out there


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## Smash (Sep 4, 2010)

Therapeutic hypothermia is not a problem unless it is done poorly. The absence of muscle relaxants AND sedation would preclude the use of hypothermia. However with adequate pharmacology it is easy to manage the patient with sedation whilst maintaining blood pressure with fluid and inotropes. Whilst the evidence does not yet exist (an Australian service is about to start a trial) it makes sense that the earlier hypothermia is instituted the better (i.e. during arrest rather than post arrest).


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