Sodium Bicarb.

Sasha

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I've asked all my instructors and preceptors, and I've gotten answers that range from "Uhhhh.. hmm.. I don't know" to "Well, our protocols say to push this much, so we do." So I'm hoping someone here can enlighten me.

I don't get sodium bicarb. You push it if someone is acidodic, correct? But with out lab values or something, which is not obtainable in the field, how do you know that by pushing sodium bicarb, it's not too much and you're not just sending them from acidosis to alkalosis? Is alkalosis less damaging to cells and tissue and such that it's a better state to be in than acidosis?
 
bicarb is a buffer, meaning it acts to resist changes in pH outside of the normal range, rather than simply raising pH under all circumstances. This is where acid/base homeostasis comes into play - the simplified version is that as the body becomes acidodic the [H]+ ions react with the bicarbonate anion to form carbonic acid and eventually water and CO2, which is blown off by the body.


HCO3- + H+ ---> H2O + CO2 (through H2CO3 as an intermediate)

If the pH shifts too much towards alkaline, the reaction operates in reverse and produces H20/[H]+. It is the nature of the chemicals that acidic conditions encourage the reaction above, and alkaline conditions encourage the reverse reaction.

Basically it's self correcting - bicarb is the bodies way of maintaining stable pH, and adding more simply increases the bodies ability to cope with excess acid.

for more

http://www.anaesthesiamcq.com/AcidBaseBook/ab2_2.php

or wikipedia
 
^
I think the key quote from that link is this:
On chemical grounds, a substance (NaH2CO3) with a pKa of 6.1 should not be a good buffer at a pH of 7.4 if it were a simple buffer. The system is more complex as it is ‘open at both ends’ (meaning both [HCO3] and pCO2 can be adjusted) and this greatly increases the buffering effectiveness of this system. The excretion of CO2 via the lungs is particularly important because of the rapidity of the response. The adjustment of pCO2 by change in alveolar ventilation has been referred to as physiological buffering.
The bicarbonate buffer system is an effective buffer system despite having a low pKa because the body also controls pCO2

Here's another good link: http://www.chemistry.wustl.edu/~edudev/LabTutorials/Buffer/Buffer.html that I found today.
 
right...a buffer will have a sort of "set point" that it will direct the pH. the set point is determined by the chemistry of the buffer itself...whatever the pH is when the acid/base reaction is in equilibrium.

The setup in the body is a bit more complicated, as the end products can all be removed or added (CO2 by respiration, bicarb via renal excretion or production...and renal activity in acid/base homeostasis is a whole topic unto itself). That allows the "set point" to be precisely controlled.

basically, what he said ^
 
right...a buffer will have a sort of "set point" that it will direct the pH. the set point is determined by the chemistry of the buffer itself...whatever the pH is when the acid/base reaction is in equilibrium.

The thing with bicarb (which I honestly didn't realize till now) is that the set point for the buffer system is about a pH below the ideal physiological point.
 
as far as I have been taught... there are 3 buffers in the body and they range from fastest reaction to slowest....Bicarb being the fastest,exhalation being the second, and renal being the third....i would never giv Bicarb unless it was a long state of cardiac arrest(due to the shutdown of the buffer system), and a TCA overdose(trycyclic antidepressant)......as for use on metabolic acidosis for any reason unknown.....i would not, just because the acid base balance is so sensitive its not worth the risk in the pre-hospital setting....my 2cents
 
To be fair, though, the renal system and respirtory system are essentially adjusting the bicarb buffer system via Le Chatelier's principle.
 
I've asked all my instructors and preceptors, and I've gotten answers that range from "Uhhhh.. hmm.. I don't know" to "Well, our protocols say to push this much, so we do." So I'm hoping someone here can enlighten me.

I don't get sodium bicarb. You push it if someone is acidodic, correct? But with out lab values or something, which is not obtainable in the field, how do you know that by pushing sodium bicarb, it's not too much and you're not just sending them from acidosis to alkalosis? Is alkalosis less damaging to cells and tissue and such that it's a better state to be in than acidosis?

God, I love the internet, Sasha. Here's what I found on emedicine's website.


http://emedicine.medscape.com/article/906440-treatment

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The general recommendation is to replace only half of the total bicarbonate deficit during the first few hours of therapy.
Do not overestimate or overcorrect the bicarbonate deficit. Rapid infusion of bicarbonate and overcorrection of the metabolic acidosis can lead to complications such as tetany, seizures, and hypokalemia by worsening the preexisting hypocalcemia and hypokalemia.
Doses of bicarbonate exceeding 1 mEq/kg per dose may lead to an alkaline overshoot. For each 0.1 increase in pH, oxygen availability may decrease by 10% because of the shift of the oxygen-hemoglobin dissociation curve to the left.
Administered bicarbonate is dissociated into carbon dioxide and water.
Carbon dioxide diffuses through the blood-brain barrier, whereas bicarbonate does not; this may lead to a paradoxical CNS acidosis.
Parenteral forms of sodium bicarbonate are available as 4% (1/2 strength) or 8% solutions. The sodium load can be significant when multiple bolus doses are administered.
If hypernatremia is a concern, consider continuous infusion of sodium bicarbonate as part of the maintenance intravenous solution. For example, 34 mEq/L of sodium bicarbonate can be added to a 0.22% sodium chloride solution to make up a 0.45% salt solution for maintenance intravenous therapy.

**********************************************************

Nothing is going to work in an either an acidic medium or an alkalotic medium. You only want to bring back balance. At least as best as possible.

Hope this helps.
 
resources that might help

not much I can add to what everyone else here has said, but if you want some good resources:

lippincotts illustrated reviews of biochemistry and pharmacology are easy reads and have saved me more than a few times.

For your instructor I suggest:

Garrett and Grisham Principles of Biochemistry with a Human Focus.
(an extremely difficult read but a suitable punishment for somebody teaching who gives you such cop out answers)
 
Just to make a point, this type of question was on a normal ACLS course (back when ACLS was legitimate 70's & 80's). One was supposed to understand the oxyhemoglobin disassociation curve and the 20:1 ratio, etc. of ABG interpretation.

My how times have changed and EMS and resuscitation requirements have been diluted and watered down.
 
I was also taught 3 mEqs in a HHN for inhalation injuries secondary to chlorine inhalation.
 
Just to make a point, this type of question was on a normal ACLS course (back when ACLS was legitimate 70's & 80's). One was supposed to understand the oxyhemoglobin disassociation curve and the 20:1 ratio, etc. of ABG interpretation.

My how times have changed and EMS and resuscitation requirements have been diluted and watered down.
double post, pay no attention to this one
 
Last edited by a moderator:
Just to make a point, this type of question was on a normal ACLS course (back when ACLS was legitimate 70's & 80's). One was supposed to understand the oxyhemoglobin disassociation curve and the 20:1 ratio, etc. of ABG interpretation.

My how times have changed and EMS and resuscitation requirements have been diluted and watered down.

The ACLS EP course isn't bad I think. it's not perfect, but I think all of those 2 day courses are not meant to teach but show people what to do until somebody who knows what to do shows up.
 
Can of worms! I like it! Short and sweet. Sodium bicarbonate is like a school voucher. It makes the numbers look better, but doesn't fix the underlying problem!

NaHCO_3 is good for hyperkalemic patients (of course with the rest of the drug box we throw at them) - but for acidosis? No - don't do it. It improves the intravascular pH but tanks the intracellular pH. Bad news. Field NaHCO_3, in my opinion should be left to hyperkalemia.

"But what if my patients acidotic -all of their enzymes and receptors are denatured - how will other drugs work?" - Well, yes you're right. Some drugs require a normal pH! So fix what's making them acidotic. Intubate them, for example.
 
Can of worms! I like it! Short and sweet. Sodium bicarbonate is like a school voucher. It makes the numbers look better, but doesn't fix the underlying problem!

NaHCO_3 is good for hyperkalemic patients (of course with the rest of the drug box we throw at them) - but for acidosis? No - don't do it. It improves the intravascular pH but tanks the intracellular pH. Bad news. Field NaHCO_3, in my opinion should be left to hyperkalemia.

"But what if my patients acidotic -all of their enzymes and receptors are denatured - how will other drugs work?" - Well, yes you're right. Some drugs require a normal pH! So fix what's making them acidotic. Intubate them, for example.

That's all good if it respiratory acidosis, but not all acidosis are respiratory. Again, treat the patient accordingly.

R/r 911
 
Just to make a point, this type of question was on a normal ACLS course (back when ACLS was legitimate 70's & 80's). One was supposed to understand the oxyhemoglobin disassociation curve and the 20:1 ratio, etc. of ABG interpretation.

My how times have changed and EMS and resuscitation requirements have been diluted and watered down.
I'm going to take a wild guess and say you were an instructor for that curriculum, too.

Anything you haven't done?




Bicarb and the acid/base balance has been a big discussion in my class on a regular basis. I understand it well enough, but I can't draw out the chemical formulas here.
 
H2O+CO2<->H2CO3<->H+ + NaHCO3
 
That's all good if it respiratory acidosis, but not all acidosis are respiratory. Again, treat the patient accordingly.

R/r 911

You're right - that's for respiratory acidosis. However, true a metabolic acidosis can't be definitively diagnosed in the field. Keep bicarb sacred!
 
You're right - that's for respiratory acidosis. However, true a metabolic acidosis can't be definitively diagnosed in the field. Keep bicarb sacred!

Neither can respiratory acidosis either yet we try to tx it. Alike respiratory, metabolic also has clinical symptomatology than indicate the need of correcting it. Also dialysis patients can be treated as one should be able to get a recent lab value.

R/r 911
 
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