US National Library of Medicine NIH: Sodium Bicarbonate Case Study

Medic27

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Link: https://www.ncbi.nlm.nih.gov/pubmed/28802878
CONCLUSIONS:
In OHCA patients, prehospital SB administration was associated with worse survival rate and neurological outcomes to hospital discharge."

What do you all think?

"SB was associated with decreased probability of outcomes (adjusted OR for survival: 0.64, 95% CI 0.45 to 0.91, and adjusted OR for favorable neurological outcome: 0.59, 95% CI 0.39 - 0.88, respectively). "

I remember observing sodium bicarb being administered during pre-hospital emergencies specifically for cardiac arrests, do you guys think is significant?
 

Tigger

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I think outside of TCA overdoses and hyperkalemia it probably has limited use. Like many things in EMS, the science makes conceptual sense (cardiac arrest=acidosis, therefore must treat with something alkaline), yet it doesn't work.
 
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Medic27

Medic27

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I think outside of TCA overdoses and hyperkalemia it probably has limited use. Like many things in EMS, the science makes conceptual sense (cardiac arrest=acidosis, therefore must treat with something alkaline), yet it doesn't work.
So imo that would render it useless, although we think it could; evidence shows against it... Is there any studies for it?
 

GMCmedic

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Studies have been back and forth on bicarb since the 1960s. AHA has been trending away from it since at least the 2010 updates.


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Medic27

Medic27

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Studies have been back and forth on bicarb since the 1960s. AHA has been trending away from it since at least the 2010 updates.


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I gotcha, I am a newer EMT so I am not entirely up to speed. Great community, thanks for the back story.
 

Tigger

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So imo that would render it useless, although we think it could; evidence shows against it... Is there any studies for it?
Well no, those are two potentially very reversible causes of arrest.
 

VFlutter

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@Tigger I think I saw a study about SB bing good for ICP, but I would have to look.

Sodium bicarb being hypertonic causes an osmotic shift similar to 3% Saline or Mannitol and can reduce cerebral edema and ICP which can be useful if you patient actually has cerebral edema but can end up being pretty harmful in a lot of situations and one of the big concerns with Sodium Bicarb use with DKA.
 
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Medic27

Medic27

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Sodium bicarb being hypertonic causes an osmotic shift similar to 3% Saline or Mannitol and can reduce cerebral edema and ICP which can be useful if you patient actually has cerebral edema but can end up being pretty harmful in a lot of situations and one of the big concerns with Sodium Bicarb use with DKA.
Why would it be bad with diabetic ketoacidosis? Could you explain? :) Thank you, I am a lot newer to the drugs outside of my scope.
 

VentMonkey

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@Tigger I think I saw a study about SB bing good for ICP, but I would have to look.
This may have been what you were referring to. If so, it's Jems, and as we both know it still leaves a lot to be desired; this is so much more of an article than a study.

http://www.jems.com/articles/print/...onate-as-a-tool-for-managing-head-trauma.html

It really seems much more practical to forego such therapies in the field without proven, and consistent EBM. Mannitol and HNS have consistently proven throughout the years to manage the brain injured patient with efficiency, sometimes we just need to stick with what we know.

Here's a publication from the latest AMJ that highlights management of brain-injured (hypertensive) patients. Much of which remains unchanged in our (prehospital) setting.

http://www.airmedicaljournal.com/#/article/S1067-991X(17)30175-X/fulltext
 

CALEMT

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@Tigger I think I saw a study about SB bing good for ICP, but I would have to look.

I know Lidocaine is the PHTLS go-to for ICP.

Since I saw someone mention cardiac arrest and SB in the 5 years I've been an EMT I've only heard of someone getting ROSC once when SB was pushed. It was an arrest at a dialysis clinic. Only time I've heard a success story with it. Other times its pushed just as a check box med during the code.
 

bakertaylor28

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My take on this is that it is absolutely meaningless, unless we know what control variables were applied within the study. Bicarb in cardiac arrest is an extremely controversial topic to begin with- and depends upon the context of the arrest- Was the patient acidic within the context of the underlying condition that caused the arrest in the first place? If so, Bicarb is going to be the quick and easy way out. If the arrest wasn't precipitated by some form or another of acidosis, it becomes that we take a closer look- as Bicarb reacts to neutralize acid, it forms CO2, which in turn, CAN feed an acidic state if we're not blowing it off. Therefore, its probably only going to be effective early on with high O2 sats.

As for neurological function- alot of this is rather subjective measurement as opposed to objective measurement, because it relies on assessment of state that is largely in the eye of the beholder, as opposed to a strict binary assessment.
 

bakertaylor28

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Why would it be bad with diabetic ketoacidosis? Could you explain? :) Thank you, I am a lot newer to the drugs outside of my scope.
It's really a moot point. When treating diabetic acidosis, your going to have a significant chance of developing cerebral edema (resulting in increased ICP) as you transition out of acidosis. In fact, it's one of the reasons that, in the long-term treatment of DKA, one should have Manitol on standby, because there's a distinct chance your going to end up having to address the issue. The notion is that Bicarb will do the reverse (and cause reduced ICP from baseline) - But in the setting of DKA the chances are that opposing forces will equal out, long term.

Where bicarb is good is when your reversing rather extreme states of primary acidosis (i.e. the acidosis is metabolic as opposed to respiratory) - because the reaction from bicarb to CO2 to carbonic acid (at least a two step chemical reaction) takes longer than it takes to bicarb neutralize the primary acid ( a one step chemical reaction.)
 
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bakertaylor28

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@Medic27 To clarify the chemical reaction, Sodium Bicarbonate reacts with an acid to form CO2 + H2O + Na. CO2 in turn will break down to form Carbonic Acid.
 

NPO

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Anecdotally, I've used Sodium Bicarbonate in one cardiac arrest, and we saw near-instant and undeniable results. However, I'm going to chalk it up to reversals causes and a temporizing measure.

The patient was a homeless man, and a known (by me from previous runs) diabetic with uncontrolled diabetes, who's BGL was always a critical high and always refused any treatment and transport, and always refused to provide information despite the previous. He was found in asystole following SCA. I took a guess, based on the limited information available (my experience with the patient). I took a shot and gave bicarb in the second round to attempt to correct the acidosis. There was a near immediate change to NSR (PEA). Next round got another epi and another bicarb with ROSC. The patient had repeated returns to PEA in the ER, also treated with bicarb and epi with ROSC each time.

We could blame the epi. But I'm leaning on bicarb for this one, unless the greats (@Chase?) can explain further.

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VFlutter

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I am by no means an expert however if the cardiac arrest is highly suspected or known to be precipitated by severe metabolic acidosis then I think Sodium Bicarb is indicated and may be beneficial to the resuscitation. The evidence isn't great either way and while routine use of Bicarb has fallen out of favor in cardiac arrest I think it is hard to argue against it with known acidosis. H's and T's, fix what you can. Also remember that in severe acidosis sympathomimetic drugs are less effective and sodium bicarb may temporarily cause a bump in pressure and output so that may have been part of the reason for ROSC.
 

Summit

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Every single patient I gave bicarb to died... push or drip... many of them... usually not right away, but within days, weeks...
There's your ICU anecdote of the day. I think it is a great temporizing measure.
I think it was more of a message that those patients that received had associated insult from the profound acidosis or its etiology that it was unsurvivable.
 
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