Seeking Perspective from the Whiz Kids!

firetender

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I'm quite tickled by the technical/scientific/medical knowledge of the medics at this site. Sometimes, I'm amazed at how knowledgeable are the contributors!

A point that surfaces again and again is the importance of applying scientific knowledge OVER the utilization of experience or intuitive judgments. Being a dinosaur, I'm curious about why all the things I did 30 years ago -- and saved lives with -- aren't supposed to work today.

Here's a simple one, taken from a call sheet dated 1/3/1978:

50 y.o. male. Witnesses state patient "just collapsed"
Pt. "probably" has history of heart related problems.
Meds - Inderal. No other info available
unconscious unresponsive at arrival of Fire Dept. Rescue
(probable 5 minute response time)
FD begins two-man CPR according to AHA standards of the day
Ten minutes later, we the paramedics arrive

Establish an airway with a Esophageal Obturator Airway (EOA)
Monitor shows asystole
CPR continued
IV D5W (500cc), 20 ga. needle, KVO (standing orders)
Push 50 mEq NaHCO3 (Sodium Bicarb) X 2 (standing orders)
follow with 10 cc 1:10,000 Epinephrine per MD's orders
Repeat 50 mEq Bicarb (at 5 minute intervals)
Repeat 50 mEq Bicarb
1 mg. Atropine I.V. push
A-V disassociation with rate of 20 - 30
Transport
On arrival at hospital A-V dissasociation with bradycardia rate about 40
No discernible resumption of breathing, but weak pulse

In my book, this was a save because we got to a patient with no heart activity and got him to the hospital with a pulse.

Can you who are much more savvy than I tell me some particulars of why this protocol is no longer in use today?
 
I do not know a whole lot as I am only a student, however here is my take....

ACLS guidelines have Sodium Bicarb as indicated for long down time/acidosis of exsisting origin, my understanding also is Sodium Bicarb may have negative effects on Epi/Atropine which are the drugs that have been proven to help outcomes.

This was a witnessed arrest with CPR in progress in less then 10minutes ACLS would have had us do EPI/Atropine, then assess H's/T's In this case D5W may be indicated however could be ruled out by getting a glucose stick, thiamine could have been indicated depending on the PT presentation of malnutrition

Only thing I can think is less of a shotgun approach?

However I have read a study that Sodium Bicarb given after getting a pulse back has improved rat outcomes
http://www.ncbi.nlm.nih.gov/pubmed/7667556
 
Did it really work?

A point that surfaces again and again is the importance of applying scientific knowledge OVER the utilization of experience or intuitive judgments. Being a dinosaur, I'm curious about why all the things I did 30 years ago -- and saved lives with -- aren't supposed to work today.

In my book, this was a save because we got to a patient with no heart activity and got him to the hospital with a pulse.

I would argue that it is not a save unless the patient is released from the hospital. I doubt in this case that the patient survived past the hospital. I had a instructor who would say that you could get hamburger to have a pulse if you push enough drugs.

In my experience, a pulse returning from asystole is rare. For each patient in which a pulse returns, how many patients in asystole that there was no pulse return? How many were harmed by the standards of that time. Pt's in vfib who were not resuscitated because of the treatment given?

Just my opinion.
 
How many were harmed by the standards of that time. Pt's in vfib who were not resuscitated because of the treatment given?

Could you expand on that please?

I find the history of mobile intensive care (ALS) quite interesting; Auckland was the third city in the world to get Paramedics in the Johnny and Roy sense behind Miami and Seattle (1969) and equal with Melbourne (Australia) in 1972.
 
I'm no expert...

Could you expand on that please?

I find the history of mobile intensive care (ALS) quite interesting; Auckland was the third city in the world to get Paramedics in the Johnny and Roy sense behind Miami and Seattle (1969) and equal with Melbourne (Australia) in 1972.

I don't have any first had knowledge and I'm not sure if there is any scientific data to support it, but have heard stories from the "Old School Medics".

How acidotic do you get by being in cardiac arrest for < 10 mins? Enough to justify pushing all of that Sodium Bicarb? What is the outcome going to be if you OD on bicarb? I know when I got into this business 18 years ago, the rescutation rate was around 0.03%. Makes you wonder if the low percentage was because of the treatment? Some agencies report a 40+% rate now using 2005 guidelines, induced hypothermia, and other new technology.

I could be wrong, but it is just my personal observation and as I stated before, just my opinion. ;-D
 
.03% is still better than 0%. sure a lot of the stuff that was done back in the day would land you in a courtroom now. this is an evolving feild, and in another 20 years im sure we will be shrugging our shoulders about some of our current standards of care...

-Jeff
 
Look at the oxyhemoglobin dissassociation curve for why we don't give bicarb by the drum anymore. If your going to have an acid-base derangement, it's arguably better to be acidotic than alkalotic.

D5 provides little increase in circulating volume after an hour or so, crystaloids have replaced it as the perfered maintnance fluid.

Epi and atropine are still first line ACLS meds.

Cardiac arrest "saves" only count if you have some form of good neuologic outcome in my book.
 
**DISCLAIMER** I am not, never have been, may never be, a whiz kid **DISCLAIMER**

There are a number of ways to answer this I guess. Ultimately what happened between then and now (and continues to happen) is evidence based practice. Much (most?) of what we do in EMS is based on 'expert' opinion, physiological rationale, ingrained habit, or because the seller of a new toy gave us a free pen. However this is slowly changing (although the rate of change is thankfully increasing) and we are demanding better evidence for what we do. However, the fact remains that much of our intervention is based on low levels of evidence.

So what does this mean? It means that, although you pushed a lot of sodium bicarbonate in this code and got a "good" outcome (although I agree with usalsfyre in regards to the meaning of 'good'), this does not mean that it was the sodium bicarbonate that did it. There are too many confounding variables (something that troubles all pre-hospital research and researchers) to say that it was the drugs. Unfortunately it is natural for us all to suffer from confirmation bias - that is counting the hits and ignoring the misses. We push some drug, and see something happen, therefore it is the drug that did it and we all celebrate, and next time we go looking for something to confirm what we think has happened or should happen.
However it may have been the other drug you gave a few minutes ago just showing some effect, it may be the 10 minutes of good oxygenation, ventilation and CPR, it could be all sorts of things. All we see and remember is "I pushed this and it worked". This is part of the reason why we need to be very careful about relying solely on our own experience and ignoring the research (see some other threads for more on this...)

Now, specifically, we gave (and some still give) sodium bicarbonate in an effort to reverse the acidosis that goes with being dead. We know that processes do not occur properly in highly acidotic environment and we know that patients in arrest are typically acidotic. Therefore reversing acidosis is intuitively a good thing, and we know that if we give sodium bicarbonate to someone they will become alkalotic. So therefore it stands to reason that sodium bicarbonate will be of benefit in cardiac arrest.

However... there are some problems with this idea. One is the fact that far alkalizing, sodium bicarbonate may in fact worsen acidosis (in the absence of effective ventilation) as it is a CO2 donor. The other part is that as IamJeff states, the oxyhemaglobin disassociation curve demonstrates that oxygen delivery is impaired in an alkalotic environment, so we may not actually be helping this either - VentMedic or someone else will be able to explain this a lot better than I can.

Ultimately though, in spite of what seems like a good idea, the data has not consistently shown a good effect from giving patients sodium bicarbonate. When the survival of those given it, and those not is compared there is not a significant difference. Therefore there is probably no point in administering it (although this is by no means without controversy)

Epinepherine is another interesting case. In the early days of resuscitation research it was discovered that effective CPR was required to improve cardiac blood flow and to improve chances of ROSC. There were some compelling animal models that showed that epi increased the chances of ROSC occuring through it's alpha-agonist effects, and this seemed to be born out in humans. However what has been discovered since is that while it may improve the likelihood of ROSC occuring, it may not improve the chances of survival subsequently, and may in fact be responsible for far worse myocardial dysfunction through it's beta effects, and probably also worse neurological outcomes (hence the interest in agents such as vasopressin - again not showing as much promise as hoped)

Equally, the change to amiodarone occured off the back of a rather underpowered study, and may have been premature (maybe not, there needs to be more research yet). Of course this is not to say that lidocaine was any use either, there are a number of reasons why this medication is probably not indicated in arrest too.

I have no doubt that as things continue to change we (or all who remain) will look back and maybe cringe a little at things we used to take as gospel. Hell, it's not that long ago that we pushed an awfully large amount of furosemide in suspected acute cardiogenic pulmonary edema; hands up who still does that any more?

Confused yet?
 
Can you who are much more savvy than I tell me some particulars of why this protocol is no longer in use today?

Sometimes patients die despite our best efforts.

Sometimes patients live despite our best efforts.

Hence the problem with case studies as anything more than a shot in the dark (when nothing else works) or a jumping off point for more research.
 
It's Out-Of-The-Box Time!

The first thing that struck me was how you guys know so incredibly much more than I ever did about the physiologic/pharmaceutical processes. Thank God! Because if I had to know this stuff, I'da kept driving the hearse!

Basically what you're telling me is Sodium Bicarb and Epi can't really, shouldn't really, or don't really convert asystole especially after 10 minutes CPR because it's been proven oxygenation is secondary to compressions fast and steady (implying taking pauses to give breaths and resume is deleterious to a successful outcome) and EOAs don't deliver much air anyway.

You're right of course! Nothing I did could have worked.

Now, I'm sorry for being so far behind, but I hear Lidocaine doesn't work. Not only that, but M.A.S.T. trousers are useless. Funny, I just finished a book about my time as a medic and it's full of success stories with this stuff.

You're right, of course! Nothing I did could have worked. But you know what? Bicarb, Epi, CPR oldkine, Lidocaine and M.A.S.T. were our mainstays at the time.

I ask you this: In the successes we had (that literally revived the dead), if they weren't attributable to the agents we used, than what did it?

Before you react, consider this: What are the odds that most of YOUR mainstays will have been debunked 25 years from now? Still, YOU GET TO SAVE LIVES WITH THEM TODAY.
 
Before you react, consider this: What are the odds that most of YOUR mainstays will have been debunked 25 years from now? Still, YOU GET TO SAVE LIVES WITH THEM TODAY.

I'm not sure if this rant was directed at me, but I'll step up to the plate on this one. The issue about treatments being debunked in 25 years is exactly my point. Sometimes due to the information available we use interventions that don't really work. We think they work when we use them, but they don't really. Those patients survive in spite of our best efforts. Similarly, we provide treatments that aren't going anywhere anytime soon and the patient dies regardless. Those patients die despite our best efforts. Nothing will change these facts, so as long as you provided the best care possible given the tools and evidence available at the time, then there's really no reason to dwell on it.

Similarly, judging something based on cardiac arrest outcomes is asking for disappointment. Cardiac arrests are the most time sensitive call that EMS gets. Unfortunately, a large number (majority?) of them are unwitnessed and the race for these patients are over the majority of time before we even get dispatched. Sure, you might pour in enough drugs and get the heart beating again. That doesn't mean that the patient had a good outcome and it doesn't mean that any treatment available then or now would have changed anything.

Also, please tell me your book isn't full of cardiac arrest "saves" that were never discharged neurologically intact from the hospital. It's like saying that you saved a house from a fire because the foundation is still intact.
 
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I'm not sure if this rant was directed at me...

Rest assured, it was not directed at anyone. At this stage of my particular game, I'm exploring a broader perspective of healing and what it's about. Writing the book led me into other trains of inquiry. Where better to offer a little musing here and there, and seek some excellent responses (like yours!) than in EMS where my explorations into the mysteries of life and death began?

And in answer to your final question, I'd have to say the outcome of any case I talk about is secondary to the larger story it illustrates.
 
The issue about treatments being debunked in 25 years is exactly my point. Sometimes due to the information available we use interventions that don't really work. We think they work when we use them, but they don't really. Those patients survive in spite of our best efforts.

Years later, as was my case, we get told they didn't really work.

The truth is, once we drop them off, for the most part we have no idea whatsoever of (and what I hear you hinting at is) the QUALITY of a life recovered. That's true for you right now. Reading a lot of the stuff on this thread, I hear that many of those early protocols were dropped because they cause collateral damage. I can't help but ask myself, despite

so as long as you provided the best care possible given the tools and evidence available at the time, then there's really no reason to dwell on it.

Just how many of my so-called saves were relegated to painful, cardiac-crippled limbos where death then became a slow, evolving process absent of any periods of productive (life-affirming) recovery?

I get to ask this stuff now so that later on, hopefully, I can share what I learned with you all and it will be useful to all of our understanding of what the work is about.
 
How many were harmed by the standards of that time. Pt's in vfib who were not resuscitated because of the treatment given?

That's a great question because it always looked like push, push, push lidocaine and v-fib worked to me (when it did!)
 
A point that surfaces again and again is the importance of applying scientific knowledge OVER the utilization of experience or intuitive judgments. Being a dinosaur, I'm curious about why all the things I did 30 years ago -- and saved lives with -- aren't supposed to work today.


Can you who are much more savvy than I tell me some particulars of why this protocol is no longer in use today?[/QUOTE]

firetender- i wish you no disrespect and i, being new to ems, have learned a lot from your contributions to this forum. but i dont understand your point.

one thing i learned immediately when i started school was there is always more to learn, especially in ems. we must strive to better ourselves and never stop. what you did 30 years ago worked and it was what you knew to do. i dont know any industry that has not changed in 30 years. it is precisely because of a greater scientific and empirical understanding that we have revised and probably improved protocols today. what you were doing then was not wrong, and you should embrace your "old school" intuition and incorporate it into current ems practices. being a new student to medicine, i dont have any intuition, all i get to do is learn today.

i guess i just dont understand your argument. do you think the old protocols are superior to present ones?
 
I ask you this: In the successes we had (that literally revived the dead), if they weren't attributable to the agents we used, than what did it?

Probably the same things that are doing it now - CPR and defib. There is still much that is unknown in medicine and in no area more so than in pre-hospital medicine: maybe some particular combination of circumstance, patient and medication along with BLS and defib was effective sometimes. Something we all do I think is to mistake improvement in physiological parameters with a good outcome - for example the desire to get a 'normal' blood pressure in a bleeding patient or a 'normal' EtCO2 in an intubated asthmatic and thinking we have done the right thing.

Before you react, consider this: What are the odds that most of YOUR mainstays will have been debunked 25 years from now? Still, YOU GET TO SAVE LIVES WITH THEM TODAY.

Given that I have not been in this industry long (12 years or so) and I have already seen much of what I took for granted debunked (fluid for penetrating trauma, M.A.S.T., large doses of furosemide for pulmonary edema, the list goes on) I think there is a very good probability that much of what I do now will not be done in the future. However, like beano, this is one of the things that I find exciting about emergency medicine and I feel it should be embraced.
 
The lost art of medicine

I mentioned this in a couple of PMs so now I guess I should just publically say it.

There is an art to medicine. We spend years hearing about isoenzymes, tolerances, receptor affinity, etc. Then particularly in emergency there is this goal to find the one size fits all miracle protocol that will raise the dead.

Indulge me:

People die from different causes. The treatments required to prevent death will vary based on the cause. (radical idea I know)

Based on epidemiology, we know what the most common causes of death are today. Based on paleopathology, chances are the diseases killing people 30 years ago may have been a little different. Logically, there were treatment plans made for those days that actually worked. As what commonly kills people changes, treatments also change.

If you play roulette, the conventional wisdom is to always bet on black. There exists the possibility that the treatments 30 years ago were based on theories that actually do work on a select number of conditions. We may have been mistaken on the mechanism of action, so the reason the treatment worked was unclear. Of course when you try to experimentally prove a treatment worked but don't know why it will likely demonstrate minimal if any effect under control. (sound like any medications you know?) So the saves were basically playing the odds to see if our treatment matched the condition. In that respect since today most "sudden death" protocols are based on cardiac etiology,did we just increased our odds of having the treatment match the patient's likely condition or did we actually figure something new out to save people?

Many of our arrest studies do have an inherent flaw of looking at treatment responding to an EKG waveform. I have yet to see one whos method looks at animals with induced DKA (or pick your pathology flavor) that progresses to v-fib and the treatment modalities of such. But does anyone doubt that the treatment based on sudden death secondary to MI is most likely different than that of another cause?

In the rush to publish, many studies simply report results and stop there. More often than not, no effort is made to identify why the suspected hypothesis doesn't prove true.

I am all for evidence based medicine. But many "studies" seem to be garbage that raise more questions than answers when you read more than the abstract and conclusion. There can even be (un)concious bias in many methods to prove a researchers point rather than an observation.

How about selection bias? "I don't want my medics to tube anymore" so I select studies that further my point, ignoring their flaws and simply ignore ones that don't say what I want.

Joseph Stalin said "quantity is a quality all of its own." I don't agree with many of his points. But a plethora of poorly done studies does not "out science" that of one good one.

We memorize our algorythms, worshipping them like some form of diety. We chant "treat the patient not the monitor." But instead of clinical findings and critical thinking. we are reduced to playing the odds on studies based on the picture on monitor.

"advanced cardiac life support" is a big lie. It is niether advanced nor life support. It is a formula to follow until somebody capable of thinking takes over. If it was worth anything at all, it would focus more on identifying reversible causes and less on "treatment order." How many can recite "H's and T's" but cannot clinically look for them? Worse yet, make up excuses on why they don't have to. If these "resuscitation" protocols actually worked, people would be discharged from the ED, the ICU would be pointless. Futhermore read the experienced provider manual. They list all kinds of treatments having "statistically insignificant" findings. But when you start adding them together, it paints a different picture. How many of us see patients that have only 1 pathology? do you have thrombus formation without ateriosclerosis? Do you have that without lipid deposit?

Does anyone else see the madness is measuring effectiveness of a treatment of survival to discharge when the whole system prior to a specialist is set up to simply buy time instead of begining to reverse the insulting pathology?

When you bet the roulette ball will land on an even number, undoubtably you may win more often but you will never win big. If you want survival to discharge, that is winning big. It will take better medical practice than a one size fits all algorythm.

I suggest treating the patient, not simply playing the odds. Unless you feel that the only people worth saving are the ones that fit into your protocol.

I hope I am around in 30 more years to see more patients saved with knowledge, procedures, and medications that make today's standards look like exorcism, hot pokers, and leeching.
 
i guess i just dont understand your argument. do you think the old protocols are superior to present ones?

By no means. I'm a bit surprised by how many of the things I thought worked have now been shown not to.
 
Slightly off topic, one of the old school medics at work was talking about Dopamine in PEA, and saying she remembers getting ROSC with that multiple times. She staid it was removed years ago and she never knew why. Anyone else remember this?

As for stuff not working, I wonder if some of the stuff we have used in the past (high dose Epi, multiple doses of bi-carb etc) does work, but only in very specific circumstances. Situations that are so specific that only a few people in a study qualify, meaning the medication statistically doesn't work.

Did that make sense?

This is a totally BS example just to illustrate my point. Magic drug A only will help people who have gone into arrest from an MI that damaged less than 40% of their heart. In a study of 1000 people, that may be why 5 of them went into arrest. So when they study Magic drug A it helps those 5 people. It helped everyone it could, but because of the overall study results, it was declared not to work.

Ok, I'm done babbling.
 
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