# Sodium Bicard admin post arrest



## rhan101277 (Jan 28, 2012)

I had a cardiac arrest patient the other day.  He was attended to by firefighters almost immediately after collapse.  When we arrived FD reports their AED shocked once.  Initial rhythm is asystole, then PEA for two rounds of CPR then I get vfib and shock at 360 and get a pulse back.  All this takes 15 minutes, I administer sodium bicarb in route thinking about acidosis and down time.  I then realize there is not protocol for doing so and that bicarb admin should be led by ABG's, which I already knew.

He had a ETCo2 of 98 which was a reason I pushed it, I did realize it was that high due to all of the downtime.  He got more bicarb after ABG showed his pH was 6.9.  Bicarb is converted to CO2 and must be blown off and since the patient is only being ventilated 8-10 a minute it could cause worsening acidosis, though it is unlikely as long as patient is being ventilated.

My FTO talked to me about to get my reasoning, he said he has never seen it done that way before.  In hindsight I should have called med control.  I didn't get into any trouble but I wanted to see what others thoughts were.


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## Smash (Jan 28, 2012)

I'm not sure I understand the rationale for giving the sodium bicarb.  If the EtCO2 is high (which is not unexpected) it is safe to assume that the PaCO2 is high, although we don't know what the gradient is without an ABG.  However, the way to fix that would be to increase your minute volume, not give another drug which is a CO2 donor.


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## NomadicMedic (Jan 28, 2012)

Did he have an ETCO2 of 98 just after ROSC? What was his ETCO2 during the arrest portion?


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## MSDeltaFlt (Jan 28, 2012)

rhan101277 said:


> I had a cardiac arrest patient the other day.  He was attended to by firefighters almost immediately after collapse.  When we arrived FD reports their AED shocked once.  Initial rhythm is asystole, then PEA for two rounds of CPR then I get vfib and shock at 360 and get a pulse back.  All this takes 15 minutes, I administer sodium bicarb in route thinking about acidosis and down time.  I then realize there is not protocol for doing so and that bicarb admin should be led by ABG's, which I already knew.
> 
> He had a ETCo2 of 98 which was a reason I pushed it, I did realize it was that high due to all of the downtime.  He got more bicarb after ABG showed his pH was 6.9.  Bicarb is converted to CO2 and must be blown off and since the patient is only being ventilated 8-10 a minute it could cause worsening acidosis, though it is unlikely as long as patient is being ventilated.
> 
> My FTO talked to me about to get my reasoning, he said he has never seen it done that way before.  In hindsight I should have called med control.  I didn't get into any trouble but I wanted to see what others thoughts were.



Rhan, 

If your protocols are anything like mine then you'll notice it says in the back in the formulary for sodium bicarbonate that you give it if pulseless for 10 min or more.  Does not say call Med Control, though the protocol doesn't even mention it at all.  But of a loop hole for you.

However, with your EtCO2 being 98, your problem was more respiratory than metabolic.  I would have bagged faster first.  Then if meds weren't working (because nothing works in an acid medium), I'd give NaHCO3.

FYI & IMHO.


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## rhan101277 (Jan 28, 2012)

Yeah it says give it if they are still is asystole or PEA, but the patient had a perfusing rhythm when I gave it.  He went 15 minutes with CPR which at best gives 2L circulation, average heart pumps 5L.

So my line of thought was that he would be acidotic because of the down time.  It doesn't seem like there would have been much difference if I gave it and he got ROSC right after or if I gave it after ROSC as long as I had good ventilations.

We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings.


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## usalsfyre (Jan 28, 2012)

rhan101277 said:


> We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings.


Are they really going to gig you for doing what an intuitive clinician would?


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## NomadicMedic (Jan 28, 2012)

rhan101277 said:


> We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings.



You don't adjust ventilations to maintain an appropriate end tidal? Then why do you use caponography? Just to verify a tube? It's so much more than that. In my opinion, caponography paints the absolute best prehospital picture of ventilation status, and if you're not adjusting your treatment after seeing numbers like an end tidal of 98, you're doing a huge disservice to your patients. Don't be a cookbook medic. Do what's right for your patients and have the knowledge and wherewithal to stand up for yourself and be a patient advocate.


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## rhan101277 (Jan 28, 2012)

usalsfyre said:


> Are they really going to gig you for doing what an intuitive clinician would?



No, I am not in any trouble for it.  I just thought I would share the story.  My FTO just wanted to make sure I had a good reason and that the treatment made since.


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## usalsfyre (Jan 28, 2012)

rhan101277 said:


> No, I am not in any trouble for it.  I just thought I would share the story.  My FTO just wanted to make sure I had a good reason and that the treatment made since.



I was saying adjusting your ventilatory rate based on ETCO2. Not doing that would be like knowing a set of directions was wrong but following them anyway because thats what's written down.


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## rhan101277 (Jan 28, 2012)

n7lxi said:


> You don't adjust ventilations to maintain an appropriate end tidal? Then why do you use caponography? Just to verify a tube? It's so much more than that. In my opinion, caponography paints the absolute best prehospital picture of ventilation status, and if you're not adjusting your treatment after seeing numbers like an end tidal of 98, you're doing a huge disservice to your patients. Don't be a cookbook medic. Do what's right for your patients and have the knowledge and wherewithal to stand up for yourself and be a patient advocate.



Think about what you posted, there are many things that cause high ETCo2 values such as low cardiac output, poor gas exchange, anxiety, COPD patients etc. 

If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.

I am definitely not a cookbook medic.


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## Handsome Robb (Jan 28, 2012)

rhan101277 said:


> If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.



True, you should be looking at the whole picture. Personally in this situation I'd say an ETCo2 of 98 after ROSC with a 15 minute downtime would indicate a tid bit of increase in ventilation rate, but that's just me.

I don't think anyone was calling you a cookbook medic...more of a statement than anything.


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## Smash (Jan 29, 2012)

rhan101277 said:


> Think about what you posted, there are many things that cause high ETCo2 values such as low cardiac output, poor gas exchange, anxiety, COPD patients etc.
> 
> If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.
> 
> I am definitely not a cookbook medic.



I think you might need to revisit the concept of EtCO2 and how it relates to PaCO2 and in turn, perfusion, ventilation, acid-base and so on.

If we go back to your original patient:

You have a patient who has arrested.  In the process of going from flow to low-flow to no flow, acidosis will of course occur.  When we get things going again, that acidosis persists as we reverse the no-flow to flow state, and metabolism starts up again, producing even more acid.
Therefore we have a lot of CO2 floating around: CO2 = acid.

Now, we don't want an acidotic state persisting, it is not good for all the enzymes and proteins and so on that need a very tight range of pH to function properly.  As the patient is not breathing on his own, he cannot use the respiratory system to blow off all that acid.  We have to do it for him.  There is no reason for that EtCO2 to stay that high if you ventilate adequately.  Assuming you are optimising perfusion with fluids and pressors/inotropes and ventilating adequately, that EtCO2 should come down nice and quickly to normo-capnic levels.  

Personally, I aim for an EtCO2 of 30-40mmHg.  In healthy person the EtCO2aCO2 gradient is usually 5mmHg, so this would give a PaCO2 of 35-45mmHg, i.e. normal.  Of course this person isn't healthy so the gradient may be quite different, but in the absence of an ABG that assumption is the best I can do.  If I were lucky enough (or smart enough) to work on one of our choppers, I would use the iStat to correlate the numbers and readjust the ventilator from there.

So your patient has high EtCO2.  In the context of what has happened, this should mean 1) he has good perfusion (you need perfusion to create CO2) and 2) he has poor ventilation (you need ventilation to get rid of CO2)

So this patient, who is ventilating poorly, is then given a drug that, in the absence of good ventilation, causes increased acidosis by donating CO2, thereby increasing acidosis.  Probably not what they need right now.

In some settings (such as the intubated asthmatic) we allow permissive hypercapnia, because the risks of trying to hyperventilate that patient outweighs the risk of allowing the CO2 to remain high for a time(we still bring it down, just not as fast).  However, not adjusting ventilation in light of EtCO2 is a very, very bad idea.


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## rhan101277 (Jan 29, 2012)

Smash said:


> I think you might need to revisit the concept of EtCO2 and how it relates to PaCO2 and in turn, perfusion, ventilation, acid-base and so on.
> 
> If we go back to your original patient:
> 
> ...



He isn't ventilating poorly, in fact after sodium bicarb admin and standard respiration rates of 10 his CO2 was down to 44 upon arrival at ED.  That is ventilating at 10/minute.


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## MSDeltaFlt (Jan 29, 2012)

rhan101277 said:


> He isn't ventilating poorly, in fact after sodium bicarb admin and standard respiration rates of 10 his CO2 was down to 44 upon arrival at ED.  That is ventilating at 10/minute.



Now we have the bigger picture.  Thank you for the information at the end of the call.  You did fine.  Good job.  Consider yourself vindicated.


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## NYMedic828 (Jan 29, 2012)

Just as a side note for my own learning,

Excess CO2 is converted into Bi-Carb in the bloodstream, and vice-versa so technically giving NaBi-Carb to a patient with Respiratory Acidosis = More CO2 and more Acidosis?

Shouldn't the cure to respiratory acidosis be respiratory and the cure for metabolic be circulatory? (ventilation/drugs)

I always had trouble fathoming the acid-base balances and buffer systems around them. Some of you guys are so ridiculously knowledgeable :/ (granted I have 3 months as a medic )

Anyone have any good links explaining it in-depth?


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## jwk (Jan 29, 2012)

rhan101277 said:


> He isn't ventilating poorly, in fact after sodium bicarb admin and standard respiration rates of 10 his CO2 was down to 44 upon arrival at ED.  That is ventilating at 10/minute.



That's actually a pretty slow respiratory rate given the high EtCO2.  There's a reason it's called "hyperventilation". 

I'm from the age where every arrest got 2 amps of bicarb before anything else.  Now we don't even give bicarb in the OR without ABG guidance, and even then, a lot of times we'll hyperventilate instead of pushing bicarb because of all the potential evils involved.


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## MSDeltaFlt (Jan 29, 2012)

NYMedic828 said:


> Just as a side note for my own learning,
> 
> Excess CO2 is converted into Bi-Carb in the bloodstream, and vice-versa so technically giving NaBi-Carb to a patient with Respiratory Acidosis = More CO2 and more Acidosis?
> 
> ...



True.  Think of it this way.  And this is straight forward and as simple as I can make it.

(Bare in mind that unless you have the luxury of temperature corrected ABG's in hand, you have no other choice but to go with this process)

The goal is to keep the pH balanced. Period.  We do this by controlling PaCO2 through EtCO2.  If EtCO2 > 45,  breathe faster. If EtCO2 <35, breathe slower.

EtCO2 has a margin of error, generally, of + or - 4-5pts.  And that depends on your pt's cardiac output and temperature (>101°/<96°).


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## NomadicMedic (Jan 29, 2012)

rhan101277 said:


> Think about what you posted, there are many things that cause high ETCo2 values such as low cardiac output, poor gas exchange, anxiety, COPD patients etc.
> 
> If you adjust ventilations just because you see a high ETCo2 number, you are doing a disservice to your patients.
> 
> I am definitely not a cookbook medic.



In a patient that had ROSC after an arrest I'm CERTAINLY going to adjust ventilations to help archive an acceptable end tidal reading. And I'm not going to push bicarb on a now perfusing patient, to "correct" an acidosis that should be fixed through ventilation. Think about it. Maybe that's why bicarb isn't in your standing orders.


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## Veneficus (Jan 29, 2012)

*surgical resuscitation (c)*



n7lxi said:


> In a patient that had ROSC after an arrest I'm CERTAINLY going to adjust ventilations to help archive an acceptable end tidal reading. And I'm not going to push bicarb on a now perfusing patient, to "correct" an acidosis that should be fixed through ventilation. Think about it. Maybe that's why bicarb isn't in your standing orders.



So what of the patient arrested secondary to DKA?

At that point, ventilation will not work as the patient has probably already hyperventilated for days if not weeks.

But the point of me illustrating this is not to split hairs, it's to point out that when resuscitating patients, when you can identify the specific pathology and treat accordingly, it doesn't make it the wrong choice if it's not directly on the protocol. 

I agree though, giving bicarb to "normalize" a post arrest patient that did not need bicarb for resuscitation while not particularly harmful may not be optimal.

Ventilation is probably the optimal choice. 

I know in every text book a big deal is made about PH, but if I could, I would just like to clarify those great minds.

Acidosis results either from a metabolic pathology (like DKA) or as a symptom of a pathology causing cells to convert to anaerobic respiration. Since that is usually caused by oxygen deficency, let's just assume that example.

During normal function, about 30% of oxygen delivered to tissue is used. Moving up to as high as 60% during extreme circumstances. When even this is not sufficent, usually because of a delivery problem, (do2) cells convert to anaerobic metabolism usually to maintain minimal life/function. 

As acid increases PH decreases, and all the wonderful things that come with that. But, before we get to the point of systemic effects, cells of the initial insult are usually in a much worse position. 

When you add the bicarb, it doesn't stop anaerobic metabolism. It only masks it. Which means you have to wait even longer to figure out if your therapies are working. If the patient is not so acute that later isn't coming.

Even small values of acidosis may point out there is still something that needs attention or intervention.

A true reading is also more useful when correlating other values in trying to get an accurate idea of what is going on. 

Anyway, the take home point is, acidosisi is usually a symptom of pathology, not often the root cause. I liken empirically treating suspected acidosis to putting skin lotion on a dehydrated person. It may seem like it is helping, but it is not what the patient needs.


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## NomadicMedic (Jan 29, 2012)

Point taken, but note I specifically said a patient with a high end-tidal following ROSC would be treated with ventilation. The patient that arrested secondary to DKA is a whole 'nother ball of wax, not particularly germane to this discussion.


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## mycrofft (Jan 29, 2012)

Nitpicky: resp rate is assumed to be normal or greater volume, and regular, and unimpeded as evidenced by absence of stridor, rhonchii, or (ausc the chest) areas of absent sounds, right? Not arguing, I am presuming.

Sidebar: back in the day, bicarb was like "mother's milk" in many minds, and pts were being received alkalinized. Alkalinated? RBC's were stingy getting rid of O2 where it was needed.


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## rhan101277 (Jan 29, 2012)

When I gave it I was thinking about down time and trying to fix acidosis quickly instead of just letting ventilation fix the problem.  I made a mistake giving it post arrest and everyone makes mistakes, I don't think it did any harm but I thought my thinking was sound when I gave it.


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## mycrofft (Jan 29, 2012)

The jury says "YES"! Good luck on the next one, done good.


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## rhan101277 (Jan 29, 2012)

SODIUM BICARBONATE (BICARB)
1.  Classification: systemic alkalizer, electrolyte buffer 
2.  Physiologic Effect: buffers H+ ions in metabolic acidosis 
3.  Major Indications: 
3.1. preexisting metabolic acidosis (perfusing patient) 
3.2. hyperkalemia 
3.3. tricyclic, phenobarbital, or aspirin overdoses 
*3.4. during cardiac arrest, after prolonged resuscitative efforts *
4.  Primary Contraindications: 
4.1. metabolic alkalosis 
4.2. hypokalemia 
4.3. simultaneously with calcium chloride 
4.4. simultaneously with catecholamines 
5.  Side Effects: 
5.1. metabolic alkalosis 
5.2. CHF (edema secondary to sodium overload) 
5.3. hypernatremia 
*6.  Additional Information: administration should be guided by arterial blood gas analysis in a perfusing 
patient...*


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## Handsome Robb (Jan 29, 2012)

So I'm not sure why you're getting defensive...you can't ask for opinions then get grumpy when they don't tell you what you want to hear.

The last post solidified the fact that you even admitted were wrong by giving it post arrest.


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## rhan101277 (Jan 29, 2012)

NVRob said:


> So I'm not sure why you're getting defensive...you can't ask for opinions then get grumpy when they don't tell you what you want to hear.
> 
> The last post solidified the fact that you even admitted were wrong by giving it post arrest.



Yeah I was, you've never made a mistake?


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## Handsome Robb (Jan 29, 2012)

rhan101277 said:


> Yeah I was, you've never made a mistake?



I never said I haven't. I make them all the time.


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## Veneficus (Jan 29, 2012)

rhan101277 said:


> Yeah I was, you've never made a mistake?



If it makes you feel any better, I don't think it was a big deal.

Like I said, perhaps not optimal, but of no negative or great consequence.


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## rhan101277 (Jan 29, 2012)

Veneficus said:


> If it makes you feel any better, I don't think it was a big deal.
> 
> Like I said, perhaps not optimal, but of no negative or great consequence.



Thanks, I read that one amp decreases pH by .1 .  I didn't think it was doing harm especially after thinking about the lab values that the internal medicine doc had when he approached me asking about the call.  The pH was 6.9 PaCo2 was 44 and bicarb was 28.  I thought it was sound thinking at the time.

Thanks for all of the replies


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## MSDeltaFlt (Jan 31, 2012)

rhan101277 said:


> Thanks, I read that one amp decreases pH by .1 .  I didn't think it was doing harm especially after thinking about the lab values that the internal medicine doc had when he approached me asking about the call.  The pH was 6.9 PaCo2 was 44 and bicarb was 28.  I thought it was sound thinking at the time.
> 
> Thanks for all of the replies



With a pH of 6.8, PaCO2 of 44, and HCO3 of 28, he had an anion gap acidosis.  Either his Na, Cl, or K is out of whack.  Post arrest my money's on K.


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## Dwindlin (Jan 31, 2012)

MSDeltaFlt said:


> With a pH of 6.8, PaCO2 of 44, and HCO3 of 28, he had an anion gap acidosis.  Either his Na, Cl, or K is out of whack.  Post arrest my money's on K.



You can't tell if there is a gap with the information given.  All you can say with those values is he has a mixed acidosis (low pH with relatively normal pCO2 and HCO3 values) unless I missed the lytes given somewhere.


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## BLS Systems Limited (Jan 31, 2012)

_"We only hyperventilate possible herniations over here, we can't hyperventilate someone based on ETCO2 readings. "_

As a respiratory therapist, I am an little concerned about the discussion of "hyperventilation".  Hyperventilation is breathing over and above what is necessary to maintain normal PCO2 to maintain normal pH.  Tachypnea is fast breathing.  If anyone is suffering from acidosis, whether its metabolic or respiratory based, increased respiratory rate normally occurs.  This is not hyperventilation.

Back in the day, we used to hyperventilate head traumas to create blow off more CO2, which decreases blood flow top the brain.  Unfortunately this decreases blood flow to the brain...


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## MSDeltaFlt (Jan 31, 2012)

Dwindlin said:


> You can't tell if there is a gap with the information given.  All you can say with those values is he has a mixed acidosis (low pH with relatively normal pCO2 and HCO3 values) unless I missed the lytes given somewhere.



Actually you have a strong indication of one going on.  Because, although It is calculated on ABG's, a bicarb of 28 and a pH of 6.8 one should have a PaCO2 a lot higher than 44; generally speaking some near 80-100.  That is me trying to do a Henderson-Hasselbach in my head, but you get my point.

Therefore, assuming those ABG's are temperature corrected (Charles's Law still works even in blood), then the only way for the pH to be that low would be for something else making the blood acidic.  Lactic acid dump off from ROSC would bring bicarb down immediately. The only other acidosis state I am aware of is anion gap acidosis.  Check the CMP.  Again my money's on K being off kilter.


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## NomadicMedic (Feb 2, 2012)

I think we might be reading too much into the original post. The OP stated he pushed the bicarb due to a high ETCO2... Nothing else. We have info that says the ETCO2 was 90 after ROSC and nothing really substantive after that. 

I still think the bicarb push after ROSC was the wrong call. I believe that the high ETCO2 most likely could have been managed with increased ventilation, not a bicarb push.


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## triemal04 (Feb 7, 2012)

Given that the patient arrived with a pH of 6.9, giving the bicarb was the correct thing to do.  Of course, it was done for the wrong reasons, which means, in essence, the OP got lucky.  That won't happen every time.

If there was a known disease process going on prior to the arrest that caused/contributed to it, then giving bicarb might be a potential treatement.  But even then, without knowing what the pH is, it's still a crapshoot.


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## KellyBracket (Mar 7, 2012)

Sodium bicarbonate - why is there so much passion around this bulky box in the code cart? 

A discussion elsewhere on the internet prodded me into looking at the 2 studies that the AHA cited as supporting the use of bicarb in out-of-hospital cardiac arrest. Pretty interesting stuff. If you want the longer review, check it out: "Sodium bicarb in a code - still no evidence." My very quick version of my review is this:

The first study really compared EMS agencies that gave bicarb early & often in cardiac arrest, versus agencies that gave it late, or not at all. Not randomized, not controlled, not nuthin'. They found that, yes, the patients treated by the the "high sodium bicarb users" tended to survive more often. The thing is, those same agencies were also better at getting in the first shock quickly, at getting in epi quickly - they generally had their s__t together. So, was it the bicarb, or was it the well-organized EMS team?

The other study compared the save rate for Seattle EMS in two time periods: from 1981-1982, and 1983-1985. In the later period, they either used epi or lido in cardiac arrest, while in the earlier period they just started a _drip_ of bicarb. The funny thing is that, while bicarb was associated with getting ROSC/admitted to the hospital, the use of "no drug" improved survival to discharge.

That's a conclusion we've seen a few times in EMS...


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## Smash (Mar 8, 2012)

I don't think there is too much passion about it. I'm fairly sure that most of us are well aware of the lack of any effect sodi bic has during arrests (or any drug for that matter)

However the OP posted a scenario where the sodium bicarbonate was used to manage post arrest acidosis, which is not an unreasonable question. 

I personally love having sodium bicarbonate, but only for certain toxicological issues.


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## TatuICU (Mar 8, 2012)

n7lxi said:


> In my opinion, caponography paints the absolute best prehospital picture of ventilation status



This is true, but if your patient is dead and you're doing CPR, then capnography readings actually tell you more about how good your CPR is as ventilation doesn't mean anything if blood is not circulating.  That said, a CO2 reading like 98 after ROSC would probably tell you that compressions were less than ideal more than it would ventilation status.


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## TatuICU (Mar 8, 2012)

Smash said:


> I don't think there is too much passion about it. I'm fairly sure that most of us are well aware of the lack of any effect sodi bic has during arrests (or any drug for that matter)



This


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## Veneficus (Mar 8, 2012)

Smash said:


> I don't think there is too much passion about it. I'm fairly sure that most of us are well aware of the lack of any effect sodi bic has during arrests (or any drug for that matter)



Why is it when you suggest it you are a hero, when I do i am a heretic?


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## Smash (Mar 8, 2012)

Veneficus said:


> Why is it when you suggest it you are a hero, when I do i am a heretic?



It must be my boyish good looks and roguish charm Vene... :rofl:

Don't worry, I get the looks at work when I suggest that intra-arrest drugs are a waste of time.  How dare I question the holy scriptures?!


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## truetiger (Mar 9, 2012)

WWMD...what would medulla do? With an ETCO2 of 98 I would suggest bagging  at a higher rate than normal. No change, then maybe bi carb.


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## KellyBracket (Mar 9, 2012)

Smash said:


> I'm fairly sure that most of us are well aware of the lack of any effect sodi bic has during arrests...



I agree; "most of us!" Not necessarily all of us, though. 

I recognize that the OP was discussing post-ROSC, but there was enough mention of intra-arrest bicarb that I felt that a brief synopsis of the weak evidence was warranted. Probably only added to the confusion!


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