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Any comments on the new study showing improved outcomes with vasopressin in asystole? Its causing quite a debate on another discussion group I frequent.
vasopressin study
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which one is that?
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Here is what was found in the EM Today verson of ACEP:
The authors found that, while there was no difference in outcomes between the two agents in the overall study, vasopressin appeared to produce better results than epinephrine for patients in asystole (but not ventricular fibrillation or pulseless electrical activity). As an aside, it is obvious that if the results are the same overall, and they are better for one subgroup, they must be worse for one or more others. The results do, in fact, show better outcomes for the epinephrine-treated groups in V. fib. and PEA, but the differences do not achieve statistical significance.
So what are the limitations of this study ? and the implications of those limitations for clinicians trying to decide whether this study should change our practice?
1. The finding of a difference in response for patients in asystole is the result of a post-hoc subgroup analysis. As we all know, the findings of a post-hoc subgroup analysis cannot be used to draw a conclusion - only to generate a hypothesis for further study in a trial in which that hypothesis is tested as a primary endpoint.
Patients in both groups received a variety of other interventions, for which the authors could not control ? nor did they attempt to do so. These certainly represent potential confounders, the influence of which cannot be elucidated with any degree of confidence.
2. The number of patients in asystole was 528 (44.5% of the total), so this subset contains a relatively small number of patients from which to attempt to derive a meaningful result. (It is actually a sizable number as resuscitation studies go, but still small.)
3. The absolute number of patients in asystole who survived to hospital discharge was 12 in the vasopressin group versus 4 in the epinephrine group. Many of us believe that the only outcome that matters is neurologically intact survival to hospital discharge. So the question, then, is how many of those twelve patients were neurologically intact? The answer is not in the paper, for reasons that are unclear. The authors use terms to describe neurologic outcome that are not defined in the paper ("good cerebral performance," "moderate cerebral disability," "severe cerebral disability," and "coma or vegetative state"). While the reader may not know exactly what these terms mean, we may surmise that the latter two groups did not have the outcome we look for in a resuscitation study, and it is entirely uncertain how many in the first two groups returned to playing Rachmaninoff. In any case, the paper offers overall numbers of survivors falling into these four categories, but no such numbers are provided for survivors of asystole.
4. If one looks at the statistical calculations for these numbers (12/257 survivors to hospital discharge in the vasopressin-treated asystole patients versus 4/262 in the epinephrine group), the P value is 0.04 and the odds ratio is 0.3. But the 95% confidence interval for the odds ratio is 0.1-1.0. As we know, when the 95% confidence interval touches 1.0, that includes the possibility that there is NO statistically significant difference between the two groups.
In summary we can say that this study generates an intriguing hypothesis: that patients in asystole may respond better to vasopressin than epinephrine, or perhaps to two doses of vasopressin followed by epinephrine. To be sure, however, this study does not answer the question of whether that hypothesis is true. The authors themselves say, "...vasopressin may be a better option than epinephrine for patients with asystole.... This post-hoc observation could be tested in a trial restricted to such patients...."
What all this means, in the view of your correspondent, is that the statement in the accompanying editorial that the findings of this study "should be translated into a new standard of care without delay" can only be regarded as sheer folly."
Don't let one of those IM freaks try to change your practice. SURVIVAL TO DISCHARGE MUST BE MEANINGFUL!
The authors found that, while there was no difference in outcomes between the two agents in the overall study, vasopressin appeared to produce better results than epinephrine for patients in asystole (but not ventricular fibrillation or pulseless electrical activity). As an aside, it is obvious that if the results are the same overall, and they are better for one subgroup, they must be worse for one or more others. The results do, in fact, show better outcomes for the epinephrine-treated groups in V. fib. and PEA, but the differences do not achieve statistical significance.
So what are the limitations of this study ? and the implications of those limitations for clinicians trying to decide whether this study should change our practice?
1. The finding of a difference in response for patients in asystole is the result of a post-hoc subgroup analysis. As we all know, the findings of a post-hoc subgroup analysis cannot be used to draw a conclusion - only to generate a hypothesis for further study in a trial in which that hypothesis is tested as a primary endpoint.
Patients in both groups received a variety of other interventions, for which the authors could not control ? nor did they attempt to do so. These certainly represent potential confounders, the influence of which cannot be elucidated with any degree of confidence.
2. The number of patients in asystole was 528 (44.5% of the total), so this subset contains a relatively small number of patients from which to attempt to derive a meaningful result. (It is actually a sizable number as resuscitation studies go, but still small.)
3. The absolute number of patients in asystole who survived to hospital discharge was 12 in the vasopressin group versus 4 in the epinephrine group. Many of us believe that the only outcome that matters is neurologically intact survival to hospital discharge. So the question, then, is how many of those twelve patients were neurologically intact? The answer is not in the paper, for reasons that are unclear. The authors use terms to describe neurologic outcome that are not defined in the paper ("good cerebral performance," "moderate cerebral disability," "severe cerebral disability," and "coma or vegetative state"). While the reader may not know exactly what these terms mean, we may surmise that the latter two groups did not have the outcome we look for in a resuscitation study, and it is entirely uncertain how many in the first two groups returned to playing Rachmaninoff. In any case, the paper offers overall numbers of survivors falling into these four categories, but no such numbers are provided for survivors of asystole.
4. If one looks at the statistical calculations for these numbers (12/257 survivors to hospital discharge in the vasopressin-treated asystole patients versus 4/262 in the epinephrine group), the P value is 0.04 and the odds ratio is 0.3. But the 95% confidence interval for the odds ratio is 0.1-1.0. As we know, when the 95% confidence interval touches 1.0, that includes the possibility that there is NO statistically significant difference between the two groups.
In summary we can say that this study generates an intriguing hypothesis: that patients in asystole may respond better to vasopressin than epinephrine, or perhaps to two doses of vasopressin followed by epinephrine. To be sure, however, this study does not answer the question of whether that hypothesis is true. The authors themselves say, "...vasopressin may be a better option than epinephrine for patients with asystole.... This post-hoc observation could be tested in a trial restricted to such patients...."
What all this means, in the view of your correspondent, is that the statement in the accompanying editorial that the findings of this study "should be translated into a new standard of care without delay" can only be regarded as sheer folly."
Don't let one of those IM freaks try to change your practice. SURVIVAL TO DISCHARGE MUST BE MEANINGFUL!
The problem with this study as well as all of the other pre-hospital or arrest studies is that the primary endpoints are always return of spontaneous circulation (ROSC) and only these "survivors" are subsequently divided into 2 or 3 groups, survival to hospital admission, 24 hour survival and survival to discharge. Recently there has been some interest in changing a secondary endpoint to include some evaluation of neurologic function.
The HUGE limitation to these endpoints is that once ROSC is obtained, the patient's care is no longer controlled!!! Think about this for a second........you could have 2 pts. with similar ROSC times and one will get aggressive goal directed therapy aimed at minimizing tissue dysoxia and further injury, while the other may be poorly resuscitated for the next 24 hours. NO STUDY TO DATE has combined ROSC endpoints with CONTROLLED, optimal post arrest resuscitation.
As someone who works both in the ER and ICU, I can tell you that when you get ROSC, the fun (and work) has just begun. In both the ER and Critical Care world, there are docs who are better at this than others. There is also quite a bit of variance since there are many ways to skin this cat and reach optimal endpoints (lactate clearance, adequate O2 delivery, adrenal axis evaluation and replacement etc....)
Until this post ROSC care is standardized to include currently known strategies to achieve endpoints of resuscitation within the first few hours, you will ALWAYS see this type of result.
Kyle
The HUGE limitation to these endpoints is that once ROSC is obtained, the patient's care is no longer controlled!!! Think about this for a second........you could have 2 pts. with similar ROSC times and one will get aggressive goal directed therapy aimed at minimizing tissue dysoxia and further injury, while the other may be poorly resuscitated for the next 24 hours. NO STUDY TO DATE has combined ROSC endpoints with CONTROLLED, optimal post arrest resuscitation.
As someone who works both in the ER and ICU, I can tell you that when you get ROSC, the fun (and work) has just begun. In both the ER and Critical Care world, there are docs who are better at this than others. There is also quite a bit of variance since there are many ways to skin this cat and reach optimal endpoints (lactate clearance, adequate O2 delivery, adrenal axis evaluation and replacement etc....)
Until this post ROSC care is standardized to include currently known strategies to achieve endpoints of resuscitation within the first few hours, you will ALWAYS see this type of result.
Kyle
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Kyle makes a great point. Part of my problem with the critcism of this and similar studies is the lack of control after the specific event has transpired.
This vasopressin trial is very similar to the amiodarone vs. lidocaine trial. The incorrect assumption made by the reader and perhaps the study designers is that once NSR is restablished, resuscitation is equivalent in each arm of the study.
To put this to an example and something that Kyle is very familiar with and could speak more to, if you have seen a septic patient resuscitated using Early Goal Directed Therapy as described by Rivers in NEJM compared to standard resuscitation protocals, you will see how largely variant this practice really is.
This vasopressin trial is very similar to the amiodarone vs. lidocaine trial. The incorrect assumption made by the reader and perhaps the study designers is that once NSR is restablished, resuscitation is equivalent in each arm of the study.
To put this to an example and something that Kyle is very familiar with and could speak more to, if you have seen a septic patient resuscitated using Early Goal Directed Therapy as described by Rivers in NEJM compared to standard resuscitation protocals, you will see how largely variant this practice really is.
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It indeed is an interesting story, and it even hit the lay press, too (it was on CNN.COM).
Big thing for me is the 95% CI that was 1.0. A lot of times this gets overlooked...
Q, DO
Big thing for me is the 95% CI that was 1.0. A lot of times this gets overlooked...
Q, DO
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I think the point about end point is one of the most crucial. Survival to discharge means little if the discharge was to a nursing home in a vegetative state.
I would also be nervous about creating a new standard of care based on one study that was a post hoc analysis. This seemed to be jumping the gun a bit.
Also, one of the things that I found odd was the use of 2 doses of vasopressin.
And then, there is actually a fourth table, which was interesting: which looked at vaspressin + epi and epi +epi.
As someone on a list serve I frequent pointed out, it appears that if anything needs to be studied, it is this comparison, as it appears that vaso + epi appears to have better outcomes than epi +epi.
Which makes sense. one of the key things that we are concerned about is coronary perfusion pressure (CPP). As was pointed out in this listserve, epi tends to over stimulate beta receptors primarily. This can induce catecholimine damage to the myocardium, whereas vasopressin, which is primarily alpha. It seems that labratory studies show improved outcomes with stimulation of alpha and beta receptors and thus vaso + epi would be the natural choice.
Looking at table 4, this seems to be borne out. What do you guys think?
I would also be nervous about creating a new standard of care based on one study that was a post hoc analysis. This seemed to be jumping the gun a bit.
Also, one of the things that I found odd was the use of 2 doses of vasopressin.
And then, there is actually a fourth table, which was interesting: which looked at vaspressin + epi and epi +epi.
As someone on a list serve I frequent pointed out, it appears that if anything needs to be studied, it is this comparison, as it appears that vaso + epi appears to have better outcomes than epi +epi.
Which makes sense. one of the key things that we are concerned about is coronary perfusion pressure (CPP). As was pointed out in this listserve, epi tends to over stimulate beta receptors primarily. This can induce catecholimine damage to the myocardium, whereas vasopressin, which is primarily alpha. It seems that labratory studies show improved outcomes with stimulation of alpha and beta receptors and thus vaso + epi would be the natural choice.
Looking at table 4, this seems to be borne out. What do you guys think?
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agreed. could use a good listserv to frequent...
Q, DO
Q, DO
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He is referring to the E-Med list serve. Sign up here:
http://www.ucsf.edu/its/listserv/emed-l/0955.html
Pelivar
http://www.ucsf.edu/its/listserv/emed-l/0955.html
Pelivar
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Used to be we could just look at a pic around here and know the gender of the person. Thanks to a certain new moderator around here that option' s no longer available. So we must all be patient with those who mistake our gender.
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Actually, that's Dr. roja. 😀
I was never good at avatars..... probably the same reason I don't have tattoos. I am not good at selecting a single 'image' that I thought "hey, yeah, that's me." But I can look at my picture and go, 'yup, that's me.'. 🙂
I have checked out the list serve and its great.
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La Doctora Roja es una chica MUY bonita...
and sassy too!
- H
P.S. My avatar is not a picture of me... but it is pretty close😀
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So I'm "a light that would eventually disclose and bring into sight all that is most hidden and secret in the universe" while riding in a Green Bugatti? 😕
Man, has this thread wandered far from vasopressin...
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I was teaching ACLS the other day to a bunch of nurses, respiratory therapists, and a couple of docs, and I almost felt guilty doing it.
We talk about all the protocols, algorithms, etc and what interventions are definitely indicated vs maybe indicated vs absolutely not indicated.
I wanted to tell them (and did to be honest) that once you get past electricity for vfib the rest of it is pretty much voodoo. In PEA and asystole, sure, you treat for reversible causes but after that they are either dead or profoundly impaired to such an extent that they will either die soon or spend their family's life savings on nursing care.
I think we should just stop after three stacked shocks and maybe one round of epi for vfib/pulseless vtach. After that it seems to me we are just kidding ourselves in the long run. You could make a case for the septic or traumatic PEA/asystole if you get them early enough in the absolute perfect conditions for resuscitation, but other than that you are just pissing into the wind. A strong wind at that.
We talk about all the protocols, algorithms, etc and what interventions are definitely indicated vs maybe indicated vs absolutely not indicated.
I wanted to tell them (and did to be honest) that once you get past electricity for vfib the rest of it is pretty much voodoo. In PEA and asystole, sure, you treat for reversible causes but after that they are either dead or profoundly impaired to such an extent that they will either die soon or spend their family's life savings on nursing care.
I think we should just stop after three stacked shocks and maybe one round of epi for vfib/pulseless vtach. After that it seems to me we are just kidding ourselves in the long run. You could make a case for the septic or traumatic PEA/asystole if you get them early enough in the absolute perfect conditions for resuscitation, but other than that you are just pissing into the wind. A strong wind at that.
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LOL.... indeed. but its these ADD traits that make EP's so much fun to work with. 😉
edinOH It is to a degree vodoo. However, it seems to me that our efforts are more for ourselves and to show the family that all as been done. Sometimes that is worth it in and of itself as it helps add some closure.
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Then let's just start pushing saline.
Sorry ma'am, but your husband has died. We did every thing we possibly could. By the way, here is your bill for the $3,000 worth of drugs we gave which we all knew wouldn't do a damned bit of good. Have a nice day. Is there somebody we can call for you?
Roja,
Don't take this personally, but your "closure" response is a load of bull****.
Sorry ma'am, but your husband has died. We did every thing we possibly could. By the way, here is your bill for the $3,000 worth of drugs we gave which we all knew wouldn't do a damned bit of good. Have a nice day. Is there somebody we can call for you?
Roja,
Don't take this personally, but your "closure" response is a load of bull****.
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I'm sorry, did you just tell me that I was full of **** but not to take it personally?
I sincerely hope that your manners with your patients is better than your manners here. Get over yourself.
Have you ever been on that other side? Ever had to deal with the closure issue outside of your own ego not being bruised because you couldn't save someone?
I pity anyone that requires more than an ounce of compassion from you.
And I pity anyone that has to work with someone who is so blinded by thier own insecurities that they jump to ridiculous and innane conclusions.
But dont take it personally.
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Me, I'm not jumping on the vasopresin bandwagon until I see more conclusive evidence of its benefit. I know the AHA is pushing it, but I've become less and less enamored of the AHA's recommendations ever since the amiodarone mess. There is exactly one medication that has been proven reliable to improve out-of-hospital outcomes in cardiac arrest. Everything else is pure conjecture and wishful thinking.
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Hmpf. Who says that the old picture wasn't me. Perhaps as a moderator, I am not allowed to portray a beautiful woman, as it will be distracting from my job...
*sigh* If I must give my title of Beauty Queen (King?) of the EM Forums, it should be given to Roja. Scrubbs would be among my top votes as well... mmm Scrubbs.
Q, DO
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I think it is VERY important to note that ACLS are guidelines only and are NOT based upon EBM.
Amiodarone does NOT increase survival to discharge (allowing for neurologically intact patients) any better than Lidocaine. AMIO simply changes the place of death...from the ED to the ICU. AMIO costs MUCH more than LIDOCAINE and is difficult to dose as it foams in the bottle.
This Vassopressin nonsense needs to be followed up with data that notes SIGNIFICANT NEUROLOGICALLY INTACT SURVIVAL ENDPOINTS!! Just as Doc Wagner noted.
Hell, at some of the hospitals I work at, they don't have RSI meds on the floors for codes...so what are the chances Vassopressin will be added any time soon?? Nil.
Amiodarone does NOT increase survival to discharge (allowing for neurologically intact patients) any better than Lidocaine. AMIO simply changes the place of death...from the ED to the ICU. AMIO costs MUCH more than LIDOCAINE and is difficult to dose as it foams in the bottle.
This Vassopressin nonsense needs to be followed up with data that notes SIGNIFICANT NEUROLOGICALLY INTACT SURVIVAL ENDPOINTS!! Just as Doc Wagner noted.
Hell, at some of the hospitals I work at, they don't have RSI meds on the floors for codes...so what are the chances Vassopressin will be added any time soon?? Nil.
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Well, a study that would show significant neuro-intact survival would have to be done in Europe only...
Thankfully the Euro is strong against the dollar so hopefully it'll happen. 🙂
Q, DO
Thankfully the Euro is strong against the dollar so hopefully it'll happen. 🙂
Q, DO
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I should have said that the concept of pursuing a bunch of questionable and most likely useless interventions when the outcome is in little doubt just for the sake of "closure" seems like a poor use of resources. I really didn't mean it personally towards you. But I understand why you took it that way. My apologies.
For the rest of your response. Get over yourself . Nice little holier-than-thou sermon you got going there on ego, insecurities, compassion etc. Good stuff.
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'questionable?' I agree that doing *overtly* reaching tactics in someone that has been down for a long time. However, using epi, shocks and cpr for appropriate rythyms is not a waste of resourses.
And your apology is really meaningless when you follow it up with *more* insults.
Feel free to chide me for continuing to considering my patients and there families. I have no intention of going up to someone and saying 'Sorry, we would have tried harder to help save your 18 year old son but he was basically brain dead when he came in. Its a waste of resourses to prolong his life even 10 hours so that you and your family could say goodbye.'
Or even, 'I'm sorry, we had other things to try but the chance that it would have worked on your <father, grandfather, mother, sister> is really small and well, its just not worth it. It cost 6000 and well, I just decided it wasn't a good use of our resourses.
So, yup, if considering something beyond the bottom line when caring for my patients (ie if within reason attempting to help family members with closure), then I will do it. And you can call me all the petty names you want.
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QuinnNSU *lol* I wouldn't dream of attempting to take your crown. It looks very fetcing on you. 🙂
And I agree that the study will probably have to come from Eur.
Freeeedom! Good point about ACLS being guidlines.
And I agree that the study will probably have to come from Eur.
Freeeedom! Good point about ACLS being guidlines.
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Both Freedom and EdinOH have made good points about the drugs used in ACLS. It is not EBM derived recommendations. The recent addition of amio is the closest thing to an EBM recommendation they got. If you try looking up a radomized controlled trial showing the efficacy of lidocaine in vf/vt you will notice that none exist. It is based on some 10 patient case study done years ago.
I understand Roja's point about the closure for patient's family. However, I would like to think that it is the EP decision as to what is "everything" we could do and not the family's. Often, I have experienced that instead of continuing to push drug after drug, you can just continue CPR while the family says goodbye. If the evidence does not even show a benefit, but it is all in theory, then I would say there is little arguement for their place in resuscitation.
Perfect example is the new studies that just came out on the use of nitric oxide synthase inhibitor in patient in septic shock. In theory, this would seem great, decrease the global hypotension, increase tissue microcirculation, all good right!
Well, the study was stopped prematurely due to increased mortality in the treatment arm compared to placebo. Apparently, by increasing their BPs, these patients died of cardiovascular complications, not MODS.
http://www.ccmjournal.com
Just something to think about.
I understand Roja's point about the closure for patient's family. However, I would like to think that it is the EP decision as to what is "everything" we could do and not the family's. Often, I have experienced that instead of continuing to push drug after drug, you can just continue CPR while the family says goodbye. If the evidence does not even show a benefit, but it is all in theory, then I would say there is little arguement for their place in resuscitation.
Perfect example is the new studies that just came out on the use of nitric oxide synthase inhibitor in patient in septic shock. In theory, this would seem great, decrease the global hypotension, increase tissue microcirculation, all good right!
Well, the study was stopped prematurely due to increased mortality in the treatment arm compared to placebo. Apparently, by increasing their BPs, these patients died of cardiovascular complications, not MODS.
http://www.ccmjournal.com
Just something to think about.
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I haven't called you any "petty names". Like I said, I apologize for my bull**** comment. It should have been stated more tactfully. As for the rest, I don't know where your conclusions regarding my ego, compassion, and insecurities comes from. I find that insulting as well.
I agree with epi, shocks and cpr as stated in my earlier post. It is the steps we take beyond those that I am skeptical about.
There is alot of lip service given to EBM and conservation of resources here and in many other medical forums. What is wrong with questioning the utility of interventions taken when ROSC is either unlikely or will only result in death in the ICU vs the ED? I question if we really are doing anything to help the pt or family in these situations, despite our most altruisitc intentions.
If there was a study published that basically concluded that all these interventions don't really mean squat when ultimate survival to discharge is measured but it sure helps the pt's family deal with their deaths, would we seriously advocate continuing them? (Such a study probably already exists in many forms actually). I guess the better question is how much should "closure" cost? Or what is the best way to help a pt's family deal with their death in an acute setting? Is it through prolonged, expensive, and ultimately futile resuscitation attempts or a caring, clear-speaking, physician who can explain well the events surrounding their death and the interventions taken?
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Your are very correct. You did not directly call me any names. You stated that my viewpoint was bull****, and the entire tone of your post was condescending and rude. I didn't think it was out of bounds to assume that your statement 'Then lets just start pushing saline' was given in the spirit of respectful discussion. My conclusions regarding your ego, etc, came directly from the patronizingly superior tone of your post that was directed towards me.
You have made incredible leaps of assumption from my statement. Your postulations regarding care have extended far beyond anything that I said. Perhaps, for whatever reason, my initial post hit a nerve with you. So, in the event that it did, I will attempt to clarify further what it was I said.
You mentioned teaching ACLS and the sensation of futility of it at times. I pointed out that at times, resuscitive efforts are often continued at times to assist in a sense of closure. I made no comments regarding procedures or actions outside of ACLS. I didn't even make a distinction between doing basic CPR and pushing drugs.
I made a point of bringing up an issue that has validity. That it is important for not only the family to have the feeling that appropriate attempts at resuscitation were made, but for the medical team caring for the patient. The level of resuscitation that is appropriatee of course varies. A child is obviously going to recieve much more agressive efforts than a 90 yo with ESRD, CAD, HTN, DM and dementia.
Regarding your statement: "If there was a study published that basically concluded that all these interventions don't really mean squat when ultimate survival to discharge is measured but it sure helps the pt's family deal with their deaths, would we seriously advocate continuing them?"
I would say that medicine does this all the time, in varying degrees, and will continue to. I am certain that you are not advocating that the only treatments that physicians initiate are the ones that have lead to ultimate survival to discharge. Terminal cancer patients are still treated for thier disease. (and I am not just speaking of pain management... Lung cancer is still treated even though the end survival rate is abysmal). The list could go on and on. The point I am trying to make is that survival to discharge is not the be all and end all. And closure is not the issue entirely either.
You are right. A physician who can explain what happened is crucial. And the part of that statement that is most crucial is the issue of caring. End of life and levels of measures taken are complicated and unique to each patient.
And I will still maintain that closure is something that is important to consider. Could someone fault the attendings who resuscitated an 18 year old status asthmaticus who was essentially braindead on arrival for getting the patient to the ICU so that the patients family could come and say thier last goodbyes? I suppose so. It could have been called in the ED. But I think they made the right decision.
It is not easy to put a price on someone elses grief and emotions. Or it shouldn't be. Unfortunately, it is a delicate balance. And putting on the proverbial 'other person's shoes' should be something that is at the back of ones mind when dealing with these issues.
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I'm not responding to just your posts specifically but rather to the larger issue at hand. You are of the opinion that closure is one of those issues. My main point is that continuing resuscitation just for the sake of being seen to be doing something either for the pt or the care team isn't necessarily the best medicine. I don't want to just start repeating my points, but that is my main premise.
This is a subject regarding acute resuscitation, not pallative care. It seems to me that survival to discharge is or should be the primary issue when dealing with these kinds of clinical situations.
I'm not a serious advocate for withdrawing all care after basic initial interventions have been attempted. I'm just brining up the point for discussion. It is something to think about.
I'm heading out of town in the morning, so enjoy the rest of the discussion.
This is a subject regarding acute resuscitation, not pallative care. It seems to me that survival to discharge is or should be the primary issue when dealing with these kinds of clinical situations.
I'm not a serious advocate for withdrawing all care after basic initial interventions have been attempted. I'm just brining up the point for discussion. It is something to think about.
I'm heading out of town in the morning, so enjoy the rest of the discussion.
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In my experience as a paramedic, we moved to Vasopressin and Cordorone right after the AHA ACLS guidlines changed. (We also use the Zoll M-series which is far superior to th LP 11 or 12, biphasic rectilinear wave form in defib and pacing, as well as holding the patent on the 40 ms pacing charge) As far as survival in VF and VT, Vasopressin and corodorne have proven superior to epi and lido as far as return of spontanious circulation. The biggest factor in survival has been the distribution of AED's and public education. Now in asystole, I personally have better resusitation success when TCP is intiated asap and bicarbonate is administered. But of all the aystolic RSC saves I've had, none of them have walked out of the hospital.
This turned out to be an interesting thread. Nice discussions about EBM and what we have in our arsenal to "stomp out disease". I know there are varying levels of training amongst our subscribers, and as you all grow as physicians, you'll see more and more people actually do come to the ED dead and should remain so. One of the most rewarding and IMPORTANT "procedures" is helping the family. We can be a very important source of closure and aid the family in any way they need.
I used the word "procedure" to describe the family meeting since we should approach the family discussion time with as much seriousness and gusto as any central line or thoracotomy. It is a skill you will develop throughout your entire career. I think it is much more rewarding to help the family than perform a triple play (intubation, central line, art line...or any other 3 combo).
Aside from this, once we get em back to ROSC, and it has been less than 30 min. We probably should cool them down. Pick your protocol, either the Bernard (Australian) or Europen protocols. They are pretty similar with good neurologic recovery.
You NEED to control for post ROSC resuscitation. The best guide is probably the one we used in our sepsis study (Early Goal Directed Therapy in the Treatement of Severe Sepsis and Septic Shock, NEJM 2001;345:1368-77, Rivers et al). Even though this was for septic patients, it was based on oxygen delivery/consumption relationships and physiologic fundamentals.
As you go through your respective residencies, fellowships and careers, remember the work only begins with ROSC, and take some extra time with the family. If you are the "bottom line" type, you can always add the family discussion time to your total Critical Care time and bill for it.
Good luck with the match,
Kyle
I used the word "procedure" to describe the family meeting since we should approach the family discussion time with as much seriousness and gusto as any central line or thoracotomy. It is a skill you will develop throughout your entire career. I think it is much more rewarding to help the family than perform a triple play (intubation, central line, art line...or any other 3 combo).
Aside from this, once we get em back to ROSC, and it has been less than 30 min. We probably should cool them down. Pick your protocol, either the Bernard (Australian) or Europen protocols. They are pretty similar with good neurologic recovery.
You NEED to control for post ROSC resuscitation. The best guide is probably the one we used in our sepsis study (Early Goal Directed Therapy in the Treatement of Severe Sepsis and Septic Shock, NEJM 2001;345:1368-77, Rivers et al). Even though this was for septic patients, it was based on oxygen delivery/consumption relationships and physiologic fundamentals.
As you go through your respective residencies, fellowships and careers, remember the work only begins with ROSC, and take some extra time with the family. If you are the "bottom line" type, you can always add the family discussion time to your total Critical Care time and bill for it.
Good luck with the match,
Kyle
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Hey Kyle,
In regards to using EGDT for post ROSC resuscitation, how effective have you found it to be with your non-septic patients?
Have there been any further studies showing the success of EGDT in both septic and non-septic patients?
Thanks
In regards to using EGDT for post ROSC resuscitation, how effective have you found it to be with your non-septic patients?
Have there been any further studies showing the success of EGDT in both septic and non-septic patients?
Thanks
No formal studies using the specific EGDT protocol in non-septic patients.
I use physiologic endpoints, similar to a modified EGDT, every day in the ICU and the ED. There have been several studies looking at variation in aggressiveness of resuscitation, the classic is Shoemaker and maximizing oxygen delivery. These all actually failed, simply because the investigators tried to drive the oxygen delivery to supranormal levels by increasing the cardiac output and little old ladies with crappy hearts couldn't do it.
One of several metaanalysis (Shoemaker Crit Care Med 2002 Aug;30(8):1686-92) looked at around 22 different studies and found that those optimizing physiologic endpoints EARLY vs. Later had improved outcomes. Heyland et al had similar findings (don't remember that reference but it was later, around 1996)
I don't know how this approach would work in trauma patients prior to taking them to the OR. Ken Mattox and Tom Scalea have both shown that "controlled" hypotension improves patient outcomes in trauma patients.
When I'm taking care of post-op surgical patients, I modify EGDT slightly, but use the same goals (SVO2 = 70, MAP > 60, CVP = 12 - 15, lactate clearing, urine output (to a point)) Notice I don't use cardiac output. The only patient population that has been shown to have mortality associated with a cardiac output of a specific number is post op CABG patients.
As you can see I can go on and on, but I won't, since I've probably bored 3/4 of the gang already. If you have any questions, please feel free to ask, on or off list.
Regards,
Kyle
I use physiologic endpoints, similar to a modified EGDT, every day in the ICU and the ED. There have been several studies looking at variation in aggressiveness of resuscitation, the classic is Shoemaker and maximizing oxygen delivery. These all actually failed, simply because the investigators tried to drive the oxygen delivery to supranormal levels by increasing the cardiac output and little old ladies with crappy hearts couldn't do it.
One of several metaanalysis (Shoemaker Crit Care Med 2002 Aug;30(8):1686-92) looked at around 22 different studies and found that those optimizing physiologic endpoints EARLY vs. Later had improved outcomes. Heyland et al had similar findings (don't remember that reference but it was later, around 1996)
I don't know how this approach would work in trauma patients prior to taking them to the OR. Ken Mattox and Tom Scalea have both shown that "controlled" hypotension improves patient outcomes in trauma patients.
When I'm taking care of post-op surgical patients, I modify EGDT slightly, but use the same goals (SVO2 = 70, MAP > 60, CVP = 12 - 15, lactate clearing, urine output (to a point)) Notice I don't use cardiac output. The only patient population that has been shown to have mortality associated with a cardiac output of a specific number is post op CABG patients.
As you can see I can go on and on, but I won't, since I've probably bored 3/4 of the gang already. If you have any questions, please feel free to ask, on or off list.
Regards,
Kyle
