# Sodium Bicarb - Re-evaulated



## 18G (Dec 13, 2010)

I found this article on Sodium Bicarb a very interesting read over on Jems.com. The author makes some great points and does a great job of relaying what the research is saying on cardiac arrest and bicarb use. 

How do others feel about Sodium Bicarb use? Do you feel its something that we should be using more than we have lately? The AHA put Sodium Bicarb on the back burner but sounds like it may deserve a second look and something providers should be reaching for more often. 

http://www.jems.com/article/patient-care/sodium-bicarbonate


----------



## Rescue911Medic (Dec 13, 2010)

18G said:


> I found this article on Sodium Bicarb a very interesting read over on Jems.com. The author makes some great points and does a great job of relaying what the research is saying on cardiac arrest and bicarb use.
> 
> How do others feel about Sodium Bicarb use? Do you feel its something that we should be using more than we have lately? The AHA put Sodium Bicarb on the back burner but sounds like it may deserve a second look and something providers should be reaching for more often.
> 
> http://www.jems.com/article/patient-care/sodium-bicarbonate



The chairman of the ECC committee thinks bicarb is useless. That's enough for me!

edit: to clarify, the AHA hasn't put bicarb on the backburner because they're bored or something, they genuinely haven't found it to be medically useful in cardiac arrest situations.


----------



## 18G (Dec 14, 2010)

The "chairman of the AHA" surely isn't the ultimate authority. You still need to research and find out answers for yourself. Don't trust fully one persons word because of a title they hold. 

Some of the studies have found it to be useful in cardiac arrest (did you actually read the article?). It's a drug that requires more thought and study when used to correct acidosis in cardiac arrest patients.


----------



## Rescue911Medic (Dec 14, 2010)

18G said:


> The "chairman of the AHA" surely isn't the ultimate authority. You still need to research and find out answers for yourself. Don't trust fully one persons word because of a title they hold.
> 
> Some of the studies have found it to be useful in cardiac arrest (did you actually read the article?). It's a drug that requires more thought and study when used to correct acidosis in cardiac arrest patients.



But he's so nice! Anyway I did read the article and it seemed to suggest that the research pretty much proves that bicarb either does nothing or is detrimental. The conclusion was "more research is needed". Kind of sounds like if it's bad we should stop giving it to people. The autopulse was cool as hell but it resulted in decreased positive patient outcomes so the ASPIRE trial was halted.


----------



## 18G (Dec 14, 2010)

Rescue911Medic said:


> But he's so nice! Anyway I did read the article and it seemed to suggest that the research pretty much proves that bicarb either does nothing or is detrimental. The conclusion was "more research is needed". Kind of sounds like if it's bad we should stop giving it to people. The autopulse was cool as hell but it resulted in decreased positive patient outcomes so the ASPIRE trial was halted.



I don't think the article was saying it was useless or mostly harmful at all. Yes, some data is showing some possible harmful effects but even more data showing it may be increasing survival. 

From the article.

... As early as 1962, researchers reported cases of patients in v fib that were in acidosis and remained refractory until the acidosis was corrected with NaHCO3. This demonstrated that it’s highly unlikely to resuscitate the fibrillating heart if severe acidosis is present.1 This has resulted in a debate over whether acidosis causes the cardiovascular system to be less responsive to medications."

... Two studies cited in the 2010 Guidelines demonstrated increased ROSC, hospital admission and survival to hospital discharge associated with the use of bicarbonate. The majority of studies showed no benefit or found no relationship with poor outcomes.

... Although the 2010 Guidelines do not recommend “routine use” of sodium bicarbonate for patients in cardiac arrest, they note that it can be beneficial in some special resuscitation situations, with a typical initial dose of 1 mEq/kg.5

... Sodium bicarbonate administration in conjunction with epinephrine was reported to increase survival as early as 1968, with more recent studies demonstrating similar results.14 This was reaffirmed in 2005 when Pittsburgh researchers found that EMS systems administering NaHCO3 with epinephrine within minutes of resuscitation demonstrated a higher ROSC, higher discharge rate and better neurological outcome.15

... Seattle continually demonstrates one of the highest survival rates for patients suffering cardiac arrest in the out-of-hospital setting. Resuscitation is reported to be as high as 45% in cardiac arrest secondary to v fib.16 Michael Copass, MD, and his colleagues have studied the effects of NaHCO3 on epinephrine and lidocaine in the outcome of cardiac arrest due to v fib, and they discovered the use of a continuous infusion of NaHCO3 led to an increased ROSC in the prehospital setting even though it doesn’t impact long-term survival.17 

... Most recently, in a 2006 study in Pittsburgh, researchers evaluated the effects of NaHCO3 administration for documented cases of cardiac arrest. Although they reported no statistical value to the early use of NaHCO3, they found value in using NaHCO3 in prolonged cardiac arrest of greater than 15 minutes. 

*Their results documented an increase in survival of prehospital cardiac arrest from 15.4% to 32.8%, which led them to question whether the decreased emphasis on NaHCO3 is appropriate.*15

... Recent interest has focused on neurological outcomes and protective measures in survivors of cardiac arrest. Researchers at John Hopkins University evaluated acidosis and brain pH of dogs during prolonged resuscitation. *The group receiving NaHCO3, cerebral pH, cerebral blood flow and oxygen consumption all remained higher at close to pre-cardiac arrest values. The group with uncorrected acidosis had significant reduction in all areas, which led the authors to conclude that cerebral acidosis was correctable by the combination of NaHCO3, adequate ventilation and good compressions.*11

... In 2002, researchers determined that cerebral acidosis occurs at a much earlier period than arterial acidosis. They concluded buffer administration during CPR promoted cerebral reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during periods of hypotension.18

... *Frequent and earlier use of NaHCO3 has been associated with higher resuscitation rates and with better long-term outcomes in prehospital cardiac arrest. The impressive improvement in outcome in the prolonged arrest group suggests that abandoning use of bicarbonate would be premature.21,22 *


----------



## Rescue911Medic (Dec 14, 2010)

I don't have the time nor the journal access to read all those sources but I'm betting that the reason the numbers vary so much is there's a low amount of participants in each study. Furthermore their conclusion was "well we should maybe think about doing it sometimes". At least in my area there's really not enough transport time anyway to consider it. Protocols around here seem to be switching towards epi and lidocaine/amiodarone only for SCA.

I dunno, I think we should be hammering down the essentials before we really delve into special cases. We need to stop interrupting/delaying CPR, shock faster, more compressions, better compressions, etc. Long-term studies with lots of participants has shown this to save lives.


----------



## Markhk (Dec 14, 2010)

18G said:


> ... Two studies cited in the 2010 Guidelines demonstrated increased ROSC, hospital admission and survival to hospital discharge associated with the use of bicarbonate. The majority of studies showed no benefit or found no relationship with poor outcomes.



Study 1 (Published 2005)
*Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate during cardiopulmonary resuscitation* (Safer Center)

Counfounding factors: Study utilized randomized escalating low-dose or high dose epinephrine, sodium bicarbonate use was NOT randomized (it was left up to the provider's judgement), study states they used 1986 AHA ACLS Guidelines (!!!), between sites bicarbonate use ranged from 3% to 98%...comparison is actually between "LOW BICARB" use sites vs. "HIGH BICARB" use sites...used data from a study conducted between 1990 to 1992. Times have changed! 


Study 2 (Published 1990) 
*Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation
* (University of Washington)

Used a historical control (shock, intubate, give bicarb infusion)  and a new protocol of giving 0.5 mg Epi or 100 mg lidocaine. Study does NOT actually look at the "Effectiveness" of Sodium bicarbonate. In fact, the EMS protocol used gave only 180 mEq of sodium bicarbonate via contineous infusion per the study authors. In fact, the paper even states, "These results should not be interpreted to show that sodium bicarbonate, a drug with potentially adverse
effects on cardiac resuscitation and hemodynamics, should be recommended for persistent ventricular fibrillation"

The quality of these two papers "cited" in ECC G2010 are actually quite poor. They are not double-blind, placebo controlled studies and reflect CPR/ACLS procedures over 20 years ago.  



> ... This was reaffirmed in 2005 when Pittsburgh researchers found that EMS systems administering NaHCO3 with epinephrine within minutes of resuscitation demonstrated a higher ROSC, higher discharge rate and better neurological outcome.15



Study 3 *Clinical use of sodium bicarbonate during cardiopulmonary resuscitation: Is it used sensibly?* (Safer Center)

This paper actually looks at the SAME clinical data as the one noted in Study 1 (again, conducted in 1990-1992)...published by the same group as well!  This time the study paper re-crunches the numbers of the clinical data to look at pattern of sodium bicarbonate use (specifically, percentage, timing and dosage). The goal of the paper was NOT to look at the effect of bicarb on survival, ONLY the pattern of use. 

Please note that the JEMS essay states that sodium bicarb use was "Reaffirmed in 2005" but the paper was actually published in 2002. (Resuscitation Volume 54, Issue 1, July 2002, Pages 47-55)  So what exactly is the author talking about the paper being "reaffirmed in 2005" ???



> ...Michael Copass, MD, and his colleagues have studied the effects of NaHCO3 on epinephrine and lidocaine in the outcome of cardiac arrest due to v fib, and they discovered the use of a continuous infusion of NaHCO3 led to an increased ROSC in the prehospital setting even though it doesn’t impact long-term survival.17



The study cited is here Study 2. Again the notion that a "continuous infusion" is important is vastly overstated, because the study authors note the infusion was slow, did not exceed 180 meq and the even the authors in the cited paper do not support the routine use of the bicarb. The conclusion in the JEMS article is not really what the paper concludes as there is no profound "discovery" with bicarb. 


> ... Most recently, in a 2006 study in Pittsburgh, researchers evaluated the effects of NaHCO3 administration for documented cases of cardiac arrest. Although they reported no statistical value to the early use of NaHCO3, they found value in using NaHCO3 in prolonged cardiac arrest of greater than 15 minutes.
> 
> Their results documented an increase in survival of prehospital cardiac arrest from 15.4% to 32.8%, which led them to question whether the decreased emphasis on NaHCO3 is appropriate.15



Again the JEMS article cites study 3, published in 2002, but talks about a 2006 study. Ummm...something is not right here. 

I have to say something is quite wrong with the citations of this JEMS article. The JEMS paper cites reference 16 for the statement, "Seattle continually demonstrates one of the highest survival rates for patients suffering cardiac arrest in the out-of-hospital setting. Resuscitation is reported to be as high as 45% in cardiac arrest secondary to v fib." but the reference actually is "How many attempts are required to accomplish out-of-hospital endotracheal intubation?", a study conducted in Pennsylvania. I'm going to look at this closer tomorrow...maybe the print version didn't transfer over to electronic...but damn, there are some glaring errors on the Jems.com site when it comes to citations. But what I am seeing here is that the cited studies in the JEMS article that claims benefit to bicarb are actually quite weak or do not actually demonstrate benefit.


----------



## Veneficus (Dec 14, 2010)

Rescue911Medic said:


> I don't have the time nor the journal access to read all those sources but I'm betting that the reason the numbers vary so much is there's a low amount of participants in each study. Furthermore their conclusion was "well we should maybe think about doing it sometimes". At least in my area there's really not enough transport time anyway to consider it. Protocols around here seem to be switching towards epi and lidocaine/amiodarone only for SCA.



I seriously worry about providers who have neither the time nor the access to become familiar with the latest in their profession.

The AHA is very good at not making any recommendations. They are also very fond of consensus. It is not that they are bad or wrong, they are an opinion. You can find that different resuscitation experts and organizations use the same studies and reach different conclusions. It doesn't make one right or wrong, but medicine deals with things that are not black and white. Because EMS often tries to simplify to "if:then" all it does is basically write off as lost patients who do not fit the protocol.



Rescue911Medic said:


> I dunno, I think we should be hammering down the essentials before we really delve into special cases. We need to stop interrupting/delaying CPR, shock faster, more compressions, better compressions, etc. Long-term studies with lots of participants has shown this to save lives.



Yes, that has been covered and advocated for years. Organizations just cathcing on are well behind. 

As for  bicarb...

Perhaps the biggest limitation of the AHA is the fact that they are not trying to make people experts. They strive for a one size fits the most solution for the least common denominator of provider until an expert can be engaged either by transporting to the expert or the expert arriving at the bedside. 16 hours of ACLS or PALS is certainly nowhere near what is required to make an expert.

Additionally if the AHA was seriously concerned with resuscitative efforts, then they would put far more emphasis on identifying and treating reversible causes. For that is really what saves patients. Not some blind algorythm for people who seriously lack education, clinical, or critical decision making skills and need a road map to be even remotely effective.

I don't have any doubt that the reason the AHA can't get the best drug for the occasion studies, is because they don't try to match drugs with indications. They just try to find the drugs that have the best odds.

I don't think it should come as a surprise to anyone that many physicians who are experts in resuscitative efforts find AHA classes to be a complete waste of time which is often required attendance by an employer or regulating agency and of no benefit.

I am not anti AHA, I just think that we have to recognize what the AHA is, does, and its limitations rather than some all knowing all powerful authority.

come to think of it, a lot of what the AHA puts out basically says "we don't really know, we need further studies."


----------



## Rescue911Medic (Dec 14, 2010)

You're worried because I don't want to read a bunch of wishy washy studies about a medication I can't even give?

I've read every CCR/Hands-Only CPR study there is, sorry if I don't feel the need to spend hundreds of dollars every year to get journal access when I can get the relevant studies e-mailed to me anyway. 

Most of this stuff is geared towards textbook SCA, yes. Know why that is? Think about your own training. You are getting bombarded with information left and right. You get your skills and practice them. Then the stuff you don't use you don't practice and you lose your proficiency. Simply put, these special cases are uncommon enough that it's better for everyone if we don't focus on them and instead hammer the essentials. Hell, we can't even do high quality chest compressions with minimal interruptions as it is, let alone mastering every little special situation. So yes, I'm going to continue to stress good high quality CPR with minimal interruptions because guess what? As a profession we still suck at it!

And yes, the AHA does tend to stray away from pushing any point too hard. It's because every time they do (re: Hands-Only CPR) people like you whine that the data isn't "conclusive enough". Every Hands-Only study there is either shows massive improvement or that it performs just as well.

edit: And believe you me, the AHA wants there to be more training. Unfortunately practically every EMS administrator in the country resists these types of changes with every fiber of their being because guess what? More training costs them more money, money that they often don't have. Here in Ohio where I live we have a ridiculous, antiquated rule which says Paramedic schools can only offer a MAXIMUM of 650 hours of training during their medic classes. Why would there ever be a limit to how much training a school can offer? Because Fire chiefs etc. don't want to pay for longer classes. The best medic schools run more like 2000 hours, which unsurprisingly produces better medics. Until we can come to a place where more training is a viable option the best patient survival rates are going to come from hammering the treatment for the most common SCAs.


----------



## Veneficus (Dec 14, 2010)

Rescue911Medic said:


> You're worried because I don't want to read a bunch of wishy washy studies about a medication I can't even give?



I stand by my original comment. EMS are either experts in emergency care and do what it takes to be so, or they are amateurs no different than a lay rescuer. 



Rescue911Medic said:


> Most of this stuff is geared towards textbook SCA, yes. Know why that is? Think about your own training. You are getting bombarded with information left and right. You get your skills and practice them. Then the stuff you don't use you don't practice and you lose your proficiency. Simply put, these special cases are uncommon enough that it's better for everyone if we don't focus on them and instead hammer the essentials.?



Actually, it is my role to learn about these exceptional cases, recognize them, and be able to act accordingly.

Personally I strive to be the best for every patient, not just the ones that make my life easier. I have also found that the limited aspect EMS is involved with is rather, well, simple. (less than 3 involved organ system pathologies really doesn't spark my interest anymore)



Rescue911Medic said:


> Hell, we can't even do high quality chest compressions with minimal interruptions as it is, let alone mastering every little special situation.



Speak for yourself. 

I think you were referring to EMS providers as a whole though. All the physicians I have encountered take proficency in their skills rather seriously.



Rescue911Medic said:


> So yes, I'm going to continue to stress good high quality CPR with minimal interruptions because guess what? As a profession we still suck at it!



Kind of sad if you ask me. Perhaps we should stop paying and funding agencies that suck at it?



Rescue911Medic said:


> And yes, the AHA does tend to stray away from pushing any point too hard. It's because every time they do (re: Hands-Only CPR) people like you whine that the data isn't "conclusive enough".



Thank you, I am rather proud of my ability to question things I hear.



Rescue911Medic said:


> Every Hands-Only study there is either shows massive improvement or that it performs just as well.



Unhijack. This thread is about bicarb.




Rescue911Medic said:


> edit: And believe you me, the AHA wants there to be more training..



Credat Judaesus Apella, non ego.




Rescue911Medic said:


> Unfortunately practically every EMS administrator in the country resists these types of changes with every fiber of their being because guess what? More training costs them more money, money that they often don't have. Here in Ohio where I live we have a ridiculous, antiquated rule which says Paramedic schools can only offer a MAXIMUM of 650 hours of training during their medic classes..



Funny that, I have been an EMS instructor in Ohio for some years and I believe that is the minimum, not the maximum. I have been involved with 2 programs that exceed the 650 by a considerable margin. They are certainly not in violation of any laws.

I have also been involved with the AHA for even longer, and one of the main purposes of their simplifications is because people who do not often resuscitate people often find too much information to be more cumbersome than useful. 

From a behavioral standpoint if I give people a simple set of instructions, they retain them longer than if I give them a long set of complicated ones. 

As well, if I make them practice it, it becomes both episodic and procedural memory which is retained longer than semantic memory.



Rescue911Medic said:


> Why would there ever be a limit to how much training a school can offer? Because Fire chiefs etc. don't want to pay for longer classes. The best medic schools run more like 2000 hours, which unsurprisingly produces better medics. Until we can come to a place where more training is a viable option the best patient survival rates are going to come from hammering the treatment for the most common SCAs.



That increased education is offered in North East Ohio today, and has been as far back as 2000. You may want to check that with ODPS.


----------



## Commonsavage (Dec 14, 2010)

First, the conclusions of this article are difficult to consider seriously when the author has a lack of understanding the basis of acidosis in cardiac arrest (the accumulation of CO2 is the primary culprit, not lactic acid).
Second, there is a considerable body of research, by others of considerably greater credibility, that shows bicarb to be of little (if any) benefit.


----------



## Veneficus (Dec 14, 2010)

As I eluded to, I think any mediciation in an arrest is pathology specific. 

Creating a study to find out if blindly administering a medication to arrest patients is going to somehow demonstrate magically bringing them back to life is going to be impossible.

I have seen a handful of patients who had both short and long term recovery with the administration of bicarb, however, as fate would have it, they had very precise causes of arrest (that we were unaware of at the time), and in all but one of the few cases (where it was the first drug given), managed to survive despite the plethora of drugs that I or we poured into them prior to reaching for the bicarb. 

But I agree, as a drug to give to every arrest, it is probably not going to help and if not indicated, will probably cause more problems.


----------



## Smash (Dec 14, 2010)

What's this I hear?  A poorly researched, badly written article in JEMS??  Say it ain't so!!! 

I hope they managed to get in a "Paramedics shouldn't be intubating" reference in there somewhere!


----------



## Veneficus (Dec 14, 2010)

Smash said:


> What's this I hear?  A poorly researched, badly written article in JEMS??  Say it ain't so!!!
> 
> I hope they managed to get in a "Paramedics shouldn't be intubating" reference in there somewhere!



You mean the tired old souls over at JEMS are not the epitomy of EMS trade publications?

I will somehow console myself with the fact I cancelled my subscription when they made their Faustian deal with the IAFC and advocate EMS providers others to do the same.


----------



## BLSBoy (Dec 14, 2010)

Rescue911Medic said:


> The autopulse was cool as hell but it resulted in decreased positive patient outcomes so the ASPIRE trial was halted.



Oh rly?
Wait for the CIRC study to come out.


----------



## BLSBoy (Dec 14, 2010)

Rescue911Medic said:


> You're worried because I don't want to read a bunch of wishy washy studies about a medication I can't even give?



Then why comment on this?
And without "wishy washy studies", we would still be calling Rampart for our 2 Amps of BiCarb on cardiac arrests. h34r:


----------



## 18G (Dec 14, 2010)

Here is another question... if sodium bicarb isn't the answer (not saying it is or isn't) than what do you feel is the best intervention for addressing acidosis in the arrest patient?

Should we focus on quality, uninterrupted compressions and appropriate ventilation rates solely to address the acidosis? What if this acidosis is directly contributing to lower rates of survival?


----------



## BLSBoy (Dec 14, 2010)

What if the acidosis was the cause of the arrest?


----------



## 18G (Dec 14, 2010)

That is possible too but the majority of cases the patient is not gonna be acidotic prior to arresting. I think regardless off which came first we need to address the acidosis and learn the best method of doing that.


----------



## Commonsavage (Dec 14, 2010)

18G said:


> Here is another question... if sodium bicarb isn't the answer (not saying it is or isn't) than what do you feel is the best intervention for addressing acidosis in the arrest patient?
> 
> Should we focus on quality, uninterrupted compressions and appropriate ventilation rates solely to address the acidosis? What if this acidosis is directly contributing to lower rates of survival?



Wow! What a novel idea!
"Yes" is the answer. As much as we would like to believe that our pre-hospital interventions are definitive care, they are not. Definitive care for critical acidosis is best given in hospital where we can have close monitoring of serum chemistries and ABGs, and access to dialysis. The prehospital application of 50 or 100 mEq of bicarb is nominal and may have little more effect than fluid Tx. Establishing effective perfusion and gas exchange (ventilation) in the field makes a world of difference.


----------



## 18G (Dec 14, 2010)

Your right but what about these patients who are severely acidotic when we pull up? Should the acidosis be addressed sooner than later? Yes, immediate CPR is starting to address the acidosis immediately by providing some perfusion, but is it possible in the field to address acidosis that is additive to just CPR?

It great to say acidosis is better treated in a hospital where more diagnostics can be utilized but until we can get the patient to point B we need to figure out what is best at point A and if there is something more that can be done.


----------



## Sandog (Dec 14, 2010)

Commonsavage said:


> First, the conclusions of this article are difficult to consider seriously when the author has a lack of understanding the basis of acidosis in cardiac arrest (the accumulation of CO2 is the primary culprit, not lactic acid).
> Second, there is a considerable body of research, by others of considerably greater credibility, that shows bicarb to be of little (if any) benefit.



Actually in the absence of O2 (as the case of cardiac arrest) cellular respiration shifts from aerobic to anaerobic. Fermentation follows glycolysis where lactic acid and ethyl alcohol are produced intracellular (Also note ATP stores are depleted thus preventing active transport of the acid out of the cell). These compounds do not disassociate in a aqueous solution very easily as does carbonic acid. Carbonic acid is unstable in serum and shifts towards its conjugate base. I would also think that compressions would play a role in mechanical expulsion of CO2 gas. I will have to do some reading up on this to be more definate.


----------



## Commonsavage (Dec 14, 2010)

Sandog said:


> Actually in the absence of O2 (as the case of cardiac arrest) cellular respiration shifts from aerobic to anaerobic. Fermentation follows glycolysis where lactic acid and ethyl alcohol are produced intracellular (Also note ATP stores are depleted thus preventing active transport of the acid out of the cell). These compounds do not disassociate in a aqueous solution very easily as does carbonic acid. Carbonic acid is unstable in serum and shifts towards its conjugate base. I would also think that compressions would play a role in mechanical expulsion of CO2 gas. I will have to do some reading up on this to be more definate.



Yes, you are correct in noting that lactic acid is a product of the anaerobic metabolism that occurs when tissues are not perfused...as in cardiac/respiratory arrest. However, the quantities of lactic acid produced are not the primary contributor to the acidosis. It is the accumulation of CO2, in the form of carbonic acid, that is THE primary contributor to serum acidosis.
By the time that lactic acid would accumulate in pathological levels, the organism/patient has reached end stage organ death.
It's fun and wonderful to see that people are thinking and exploring the basic science behind what we do. Keep in mind what we do is PRE-hospital medicine. Critical lactic acidosis requires dialysis. My service, although progressive, is cheap and won't give me the latest greatest portable dialysis unit.


----------



## usalsfyre (Dec 14, 2010)

18G said:


> Your right but what about these patients who are severely acidotic when we pull up? Should the acidosis be addressed sooner than later? Yes, immediate CPR is starting to address the acidosis immediately by providing some perfusion, but is it possible in the field to address acidosis that is additive to just CPR?
> 
> It great to say acidosis is better treated in a hospital where more diagnostics can be utilized but until we can get the patient to point B we need to figure out what is best at point A and if there is something more that can be done.



Given the choice, it is better for the critically ill to be slightly acidotic rather than alkalotic. Without lab values to guide therapy directed at correcting acidosis, it is easy to overshoot and end up alkalotic. 

If you have reason to believe the arrest was primarily caused by a primary METABOLIC acidosis, than bicarb is certainly approprite. Otherwise, probably best to use CPR.


----------



## 18G (Dec 15, 2010)

> Given the choice, it is better for the critically ill to be slightly acidotic rather than alkalotic. Without lab values to guide therapy directed at correcting acidosis, it is easy to overshoot and end up alkalotic.
> 
> If you have reason to believe the arrest was primarily caused by a primary METABOLIC acidosis, than bicarb is certainly approprite. Otherwise, probably best to use CPR.



I have heard this same thing somewhere else too... the preferred acidosis over alkalosis. I just found the article interesting and some of the study data in the article I had not seen before and some of it was intriguing to me and made sense as to why it may be beneficial. I am a rather new Medic so I have not used bicarb ever unlike a few of you that have prob used it by the gallons back in the day (least from what I hear).


----------



## 18G (Dec 15, 2010)

Commonsavage said:


> However, the quantities of lactic acid produced are not the primary contributor to the acidosis. It is the accumulation of CO2, in the form of carbonic acid, that is THE primary contributor to serum acidosis.



Lactic acid gets converted to CO2. So one can expect with lots of lactic acid high levels of CO2 will prevail. When perfusion is restored the lactic acid is converted back to pyruvate which than continues on in the normal process of cellular respiration. 

If you want to get specific isn't it really the hydrogen ion concentration that leads to acidotic effects and is what triggers certain physiological changes in the body? Since CO2 breaks down into hydrogen?


----------



## socalmedic (Dec 15, 2010)

BLSBoy said:


> Then why comment on this?
> And without "wishy washy studies", we would still be calling Rampart for our 2 Amps of BiCarb on cardiac arrests. h34r:



well not rampart, but Bicarb is a base order for cardiac arrest for me, so is dextrose. i feel that i work in a "progressive" county, the medical director feels that those drugs are of no use in an arrest. hell i dont even check a blood sugar because there is nothing i am going to do for it until i get pulses back.

point of the story is that maby these "wishy washy studies" are actually telling us something, and are definitely telling the guys who went to many more years of school and get paid way better than us how to write our protocols. 

 blsboy this statement wasn't pointed at you, i just wanted to put a reference to my post above.


----------



## socalmedic (Dec 15, 2010)

Sandog said:


> Actually in the absence of O2 (as the case of cardiac arrest) cellular respiration shifts from aerobic to anaerobic. Fermentation follows glycolysis where lactic acid and ethyl alcohol are produced intracellular...



I am fairly certain that we do not ferment (the enzymes needed are not present), we do undergo anaerobic respiration. they are not the same. glycolisys and a shortened version of the crebs cycle are still present.


----------



## Sandog (Dec 15, 2010)

Commonsavage said:


> Yes, you are correct in noting that lactic acid is a product of the anaerobic metabolism that occurs when tissues are not perfused...as in cardiac/respiratory arrest. However, the quantities of lactic acid produced are not the primary contributor to the acidosis. It is the accumulation of CO2, in the form of carbonic acid, that is THE primary contributor to serum acidosis.
> By the time that lactic acid would accumulate in pathological levels, the organism/patient has reached end stage organ death.
> It's fun and wonderful to see that people are thinking and exploring the basic science behind what we do. Keep in mind what we do is PRE-hospital medicine. Critical lactic acidosis requires dialysis. My service, although progressive, is cheap and won't give me the latest greatest portable dialysis unit.



Not to beat a dead horse but to make one final point. According to the Trauma triad of Death. 

Quoting Wiki 


> In the absence of blood-bound oxygen and nutrients (hypoperfusion), the body’s cells burn glucose for energy (lactic acidosis), which in turn increases the blood’s acidity (metabolic acidosis). Such an increase in acidity can reduce the efficiency of the heart muscles (myocardial performance), further reducing the oxygen delivery and hence triggering a deadly cycle.



http://en.wikipedia.org/wiki/Trauma_triad_of_death

Another source.
http://www.meridianhealth.com/m/pdf/TraumaTriadShock.pdf

Well I will see what else I can dig up.


----------



## Sandog (Dec 15, 2010)

socalmedic said:


> I am fairly certain that we do not ferment (the enzymes needed are not present), we do undergo anaerobic respiration. they are not the same. glycolisys and a shortened version of the crebs cycle are still present.



Well quoting from one of my biology textbooks.

Human cells make ATP by lactic acid fermentation when oxygen is scarce.

From glycolysis, pyruvate is reduced by NADH to form lactate (Ionized form of lactic acid). 

C3H3O3 + 2NADH ---> C3H5O3 + 2NAD

"Biology 7ed. Campbell and Reece pp174-175.


----------



## Veneficus (Dec 15, 2010)

Commonsavage said:


> Yes, you are correct in noting that lactic acid is a product of the anaerobic metabolism that occurs when tissues are not perfused...as in cardiac/respiratory arrest. However, the quantities of lactic acid produced are not the primary contributor to the acidosis. It is the accumulation of CO2, in the form of carbonic acid, that is THE primary contributor to serum acidosis.
> By the time that lactic acid would accumulate in pathological levels, the organism/patient has reached end stage organ death.
> It's fun and wonderful to see that people are thinking and exploring the basic science behind what we do. Keep in mind what we do is PRE-hospital medicine. Critical lactic acidosis requires dialysis. My service, although progressive, is cheap and won't give me the latest greatest portable dialysis unit.



Where to begin...

Ok, since it would take no less than a book to explain all of this, and I have no intention of writing one, let me try to point out a few key problems here.

Bicarb is the major buffer system of the serum. RBCs in the serum are subject to acidosis in the form of protein denaturing and enzymatic alteration of normal function.

Irrespective of the effects of end organ lactic acidosis, losing the ability to carry and donate oxygen molecules ends in organ damage.

Because the RBCs do not use TCA as a substrate producing path, they are particularly vulnerable because they are already using lactic acid metabolism.

Brain cells requiring oxygen in high concentration to get substrate primarily from the TCA cycle are dependant on this o2 transport and delivery. For a bit, there is alterantive sources for brain, but it is rather a short time.

Then you have the issue of renal papilae being rather vulnerable to oxygen deprivation. Once they start to denature, slough, and die, there can be a sequele of renal dysfunction (I'd love to explain it, but like I said I am not writing a book)

When the area surrounding the hepatic venous system loses it's meager oxygen supply, it also contributes to hepatic dysfunction in a short time. The conventional wisdom was that since hepatocytes can regenerate this was not a major issue. However, I am hoping to win my Nobel in medicine demonstrating that temporary liver dysfunction impacts the rest of the ability of the total organism to compensate in the periarrest state, when liver products are absent or altered. After all, what good is a heart full of oxygen without fatty acid metabolism? Of course what good is any organ if you have oxygen but no substrate?

Once bicarb and phosphate buffers are overloaded or in effective, it takes the body days to adjust. (providing the kidneys are functioning) In the meantime you have RBC permiability if not lysis. (for a variety of reasons like shape and structural integrity) Once the membrane is permiable, you start to lose adenosine. (which if you need atp, is going to be a really big problem)

Moreover, once you have mitochondrial membrane leakage in any mito. containing cell, irresgardless of the PH level, the caspase cascade is going to finish off the cell. (think of it at a grand level like in megaMoles or gross organs)

and i will not bother to type ot the systemic inflammatory sequele except to mention it also plays a part.

This is why the whole cardiac arrest algorythm will never get survivial beyond its epidemilogical value. It is why all the studies showing the benefit or lack of specific drugs are inherintly flawed. Because you are hoping your subjects pathology falls into your treatment, rather than targeted treatments to specific pathology. 

Have you ever seen a study that shows the effects of bicarb on patients in cardiac arrest secondary to DKA? I haven't.

Or epi in hypertensive crisis secondary to pheocrhomocytoma?

Or amiodarone in arrest secondary to hyperkalemia?

But instead they pick things identifiers like V-fib. Which may or may not correlate sometimes. I wonder about the quality of the professionals that pick extraordinarily vague parameters like this for studies.

It is why all of us old gys have anectdotes about seeing bloodletting and cautery save lives  or some studies show minor benefit and some show harm. If you read these studies regularly, you will notice the pathology report is never included. (if even performed) 

In the publish or perish environment of evidence based medicine, most studies are not worth the paper they are printed on. It is why clinical judgement and proficency along with sound demonstrated basic scientific knowledge is what will be required to save lives. 

Anything less is just a trial and error, with saves being accidents rather than definitive care.

While I agree that the ICU in a hospital is more suited to saving lives than the back of a truck on the street, it is important to remember that in coaglative necrosis, the time period is about 4 days. So what happens in the truck on the street that is not apparent or easily demonstratable, directly affects the sequele once the pt. gets to the ICU. The reason survival to discharge is so low, is becase by the time the pt. makes it to the ICU, the irreversible cascades have started and the deal was done 8-20 minutes into the prehospital phase.

I once had the idea we could be more effective by moving this intensive medicine into the earlier stages of care like the field or ED. But there was so much resistance to it from field providers, I gave up.


----------



## zmedic (Dec 15, 2010)

I would point out that if the hospital isn't using Bicarb doesn't help the severe acidosis before a cardiac arrest, it isn't going to magically save the patient when they are now much sicker and have no pulse. Look at how most of these acidotic conditions are treated in the hospital. DKA gets fluid and insulin, sepsis gets antibiotics and fluids, toxic alcohols get ETOH or fomepazole etc. One of the only things that gets Bicarb is aspirin OD or TCA OD (the second is now pretty rare.) But in ASA the patient is alkalotic from the respiratory alk even though they also have a metabolic acidosis. 

So even though it would make sense to correct the acidosis in cardiac arrest, improving perfusion and ventilation is going to have a much bigger effect on pH than a few amps of Bicarb. 

As to getting more aggressive with prehospital treatment, I'm getting discouraged. There are some truly excellent providers out there, but most people I've seen seem to still be working on the "basics" of critical care like intubation, uninterupted compressions, ECG reading etc. And unless it was very protocol driven I'm not sure the average medic in the US is ready for all those spicy things like central lines and antibiotics. I wish they were. I think it is easy as a medical student or doctor who does EMS to say "we should be able to do these things in the field." But there has to be a line where you say that some things should be done by those with high levels of training.


----------



## Veneficus (Dec 15, 2010)

zmedic said:


> As to getting more aggressive with prehospital treatment, I'm getting discouraged. There are some truly excellent providers out there, but most people I've seen seem to still be working on the "basics" of critical care like intubation, uninterupted compressions, ECG reading etc. And unless it was very protocol driven I'm not sure the average medic in the US is ready for all those spicy things like central lines and antibiotics.



I agree with what you are saying, but I am of the mind that eliminating the poor performers would be a giant step in the right direction. I think the best way to do that is by making EMS a minimum of a 4 year degree. But since obviously that is not going to happen in the US, we might as well just make the current providers feel better by giving them some toys to abuse the corpses with and every now and again get a save inspite of the interventions.



zmedic said:


> I wish they were. I think it is easy as a medical student or doctor who does EMS to say "we should be able to do these things in the field." But there has to be a line where you say that some things should be done by those with high levels of training.



I think that goes hand in hand. I see the European doctors in the field and it is truly inspiring to watch. But since even most physicians involved in US EMS have no desire to spend anymore time on EMS than they absolutely have to, I expect the US to fall further and further behind in relation to EMS effectiveness, value, or even usefulness.

You are right, there is a line, it has already been drawn, and it should be performed by more capable providers. The trouble in the US is there simply isn't any appreciable quantity of more capable prehospital providers.

But the crap passing for published studies in regards to EMS treatments isn't doing much to further the field either. Have to get some garbage with a name on it for residency application right?


----------

