Just returned from Castlefest 2013–best ultrasound conference ever!
So last podcast, I bashed on sodium bicarbonate or as John Kellum and David Story call it: chloride-free sodium. This episode I talk about all the good reasons to use NaBicarb. This is part of a series
- Part I lays out the background of the quantitative approach
- Part II puts it in mathematical terms to allow calculation of acid base status
- Part III takes you through some real world examples
- Part IV discusses the Acid-Base Effects of IV Fluids
- Part V down with the Bicarb
- Part VI is this one: ok, bicarb is not all bad
The Acid Base Series
- EMCrit Podcast – Acid Base Ep. 7 – Bicarb Updates, Quantitative Approach, and Prof. David Story
- Podcast 97 – Acid-Base VI – Chloride-Free Sodium
- Podcast 96 – Acid Base in the Critically Ill – Part V – Enough with the Bicarb Already
- EMCrit Podcast 50 – Acid Base Part IV – Choose the Solution Based on the Problem
- EMCrit Podcast 46 – Acid Base: Part III
- EMCrit Podcast 45 – Acid Base: Part II
- EMCrit Podcast 44 – Acid Base: Part I
A physiology quandary
Owen, an anaesthesia registrar, wrote with this comment:
[…On increasing minute ventilation on vented patients with any bicarb given: Great idea and probably what most of us do, but even if you don't then with each breath the patient will be getting rid of more CO2 than previously so there should be more weak acid loss.]This is one of those situations where I was gobsmacked for a second. When I started to think about this, it seemed intuitively wrong and yet conceptually right. I knew I needed to find someone far smarter than me. I reached out to Mel Herbert, who recommended David Story. Dr Story is Chair of Anaesthesia at the Melbourne Medical School and a physiology god. Here is his response:
Dr. Story, Here is the quandary. As you saw, I did that acid-base show with Dr. Kellum discussing NaBicarb use for the critically ill. Both Dr. Kellum and I believe and the evidence bares out that in a patient who can't get rid of the excess CO2, there will be negligible changes in pH from the bicarb administration.Now in an apneic patient, I think this is inarguable. However, in a mech. ventilated patient with no resp drive (let's say a pt we gave NMBs to), I perpetrated the situation would be the same. In response of my listeners brought up this question: If the minute ventilation is kept the same, but the ETCO2 rises (and by extension, the return of CO2 to the alveoli), this would seem to indicate that each breath is actually eliminating more CO2. Say the ETCO2 went from 40 to 80 with the same Vt. Is more CO2 being eliminated and if so, would this alone clear the transitory excess CO2 from the bicarb? This made me think of the opioid overdose patient. As their CO2 rises, are they too eliminating more CO2 with each of their breaths? My cursory understanding has always been simply that CO2 elimination is directly proportional to minute ventilation. That is what i took from West and never really gave it much thought. Now I am thinking and it is puzzling. –Scott
Response from Dr. Story: I agree it is confusing but this is how I see it. I wrote a letter the Anesthesiology years ago on a related topic.
The short answer is it is all relative.
The universal alveolar air equation for any gas (x) is:
PAx = PIx +/- Vx / VA; where PA is alveolar partial pressure, Vx is production or consumption of the gasFor an excreted gas like CO2 this will be:
PACO2 = PICO2 + K (VCO2 / VA)The constant is due to VCO2 being STPD and VA being BTPS and is about 800 if you are using mmHg and ml/min.
So usually PACO2 = 40, PIcO2 = 0, VCO2 = 250 ml/min and VA = 5,000 ml / min (10 X 500ml)
Also PACO2 is directly proportional to VCO2 and inversely to Va.
Now if we give NaBic and Bic forms CO2 VCO2 will increase. If it went up 50% it would be from 250 ml / min to 375 ml / min. If VA is fixed then
PACO2 = 800 X 375 / 5,000 = 60 mmHgHowever I agree that Va will go up which will be due to the increase in VCO2, ie the EXPIRED VA will increase
(inspired unlikey = expired when VO2 does not equal VCO2, that is the respiratory exchange ratio does not equal 1, that is what the F in the alveolar gas equation corrects)
Therefore the VA is now 5,125 ml / min
PACO2 = 800 (375 / 5,125) = 58.5 mmHg.
We have had a 50% increase in VCO2 but only a 2.5% increase in VA this will lead to a new equilibrium point in alveolar and arterial CO2 at around 58mmHg.
I have exaggerated the effects of NaBic or as I call it chloride-free sodium to demonstrate the effects as I see it.
Therefore, yes the alveolar ventilation increases due to greater CO2 excretion but it is a relatively small effect on VA. To reduce the PACO2 back to 40 will require a 50% increase in VA. This will be transient as the VCO2 returns to the rate prior to the NaBic infusion.
I hope the above helps. If not let me know.
Cheers
Dave Story
So what do I take from all of that? I think regardless of any increase in minute ventilation, the CO2 will eventually go back to baseline after an adminsitration of sodium bicarbonate and you will see the alkalizing effect, but unless you increase the minute ventilation it will take much longer.
Use of Sodium Bicarbonate
If not stored in glass, bicarb containing solutions exchange CO2 and become not so much bicarbonate.
When to use Bicarb
- Na Channel Blockade in Tox (Slow Push; Hyperventilate if on Vent)
- Alkalinization for Tox, such as Salicylate Toxicity (Slow Push and then Drip; Hyperventilate if on Vent) [Thanks, Ben!]
- Non-SIG Acidosis (Drip or IV Fluid)
- SIG Acidosis (As an IV Fluid)
- Increased ICP (Drip)
- Hyperkalemia (As an IV Fluid)
- Hyponatremia (Drip)
ICP
NaBicarb can be used as a substitute for hypertonic saline in increased ICP (Neurocrit Care 2010;13:24 & Neurocrit Care 2011;15:42). They used 85 ml of 8.4% sodium bicarb infused over 30 minutes.
Why use Isotonic Bicarb as an IV Fluid?
Read this article by Ed Omron (J Intensive Care Med. 2010;25(5):271-80.)
Problems with Bicarbonate Drips
- Hypokalemia
- Hypocalcemia
When not to use Bicarb
- Probably no role in Cardiac Arrest unless you feel the patient has hyperkalemia or toxicologic cause.
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Scott Weingart
Hello EMCrit Crew, I’m not sure if you still reply to comments this far back but I had a question on the use of Sodium Bicarbonate for hyponatremic seizures. Speaking prehospitally, If you had a patient with seizures refractory to benzos, and reason to suspect hyponatremia as the cause, could prophylactic use of Nabicarb be justified? What are other potential etiologies I could disturb if the cause was not due to hyponatremia?
Thanks a lot
Maalox is cheaper than bicarb for smelly feet
Messier though. I like just squirting the bicarb on the socks from afar.
Did you mention bicarbonate use in salicylates ?
Great Add Ben!
Pre-intubation reasons???
Ummm, that was addressed in the last podcast. It doesn’t work for that purpose.
Hi Doc, curious. The podcast done last year with the LVAD gents from CA stated CPR wasn’t necessarily contraindicated with LVAD placement. But the new REMAC protocol is very specific about chest compressions not being done. Has there been a change in the science or new data in regards since the original podcast?
Thank you.
All depends on who you ask.
Doc, here is my expanded thoughts on crush injuries while you await response from Cliff Reid..
I’ve been taught, but never done it, that patients with an entrapped limb need to get 50-100mEq prior to compression being removed via push dose, or drip to combat potential hyperkaeleimia, and otherwise, general acidosis from the cell death that has occurred in the entrapped limb.
Post push dose, or drip dose of sodium bicarb, we were always instructed to do 50mEq per L of saline, and infuse it over an hour. My thoughts are…
A. Is it underdosed?
B. Does it actually solve anything, or is it just a bandaid solution
C. Do we have the same issues seen in crush injuries, that we may see with tourniquet use? (I fully support tq use)
Hi Ryan
I frequently debate this with colleagues. In the absence of evidence, we end up agreeing to disagree.
My view is that the practice of infusing bicarbonate prior to release of an entrapped victim in order to prevent dysrhythmia is bollocks.
Happy to go into more detail as to why if you like.
Cheers
Cliff
Cliff,
After listening to the past two shows, I feel like I can understand why it likely won’t work, but, I’d love to have you expand on it. Ether on Scott’s show, or here…
Thanks!
Cliff,
Mechanistically, it would seem to make more sense to give these folks an amp of CaCl before removing the objects from crushed extremity. Is anyone doing this?
s
Our protocols recognize both 1g CaCl and 1-2 amps NaBicarb prior to releasing a crush-injured patient.
I finally had a chance to review our protocols after my vacation….ours simply states, 50mEq in 1000mL bag of NS, infuse W/O…nothing further as to why, when, or followup after…
I’ll have to look into this and see if this got missed on our last revision.
HI
I have learn from the PHTLS 2007 that patient with crushed injuries need calcium + sodium bicarbonate 1 amp/1L prior to compression being removed. That is because of the large released of potassium and myoglobin from the muscle intracellular space of the crushed tissue in the circulation. The bicarbonate is used to alkalised the urine and prevent the formation tubular casting from myoglobinuria.
Is this still make sense?
There’s a podcast who talks about it too
http://burndoc.libsyn.com/traumatic_rhabdomyolyisis_crush_syndrome
thanks
Hi Scott.
When you give bicarbonate as a push over 10 minute push, how do you have it administered? Do you have the nurse stand there and do it?
Oops, just listened again and heard the 2 amps in 100 mL NS.
Hi Scott,
I’m an emergency medicine resident and I had an odd situation the other day. Patient with past medical history of diabetes and chronic pancreatitis came in with nausea, hematemesis, and abdominal pain. Workup showed a blood sugar of 563, hypokalemia, hyponatremia, hypochloremia, an anion gap of 15, ketones and glucose in the urine but no acididosis (albumin was around 4, coags were normal). I know there are a few conditions that can cause an elevated anion gap without an acidosis, though I’m not sure what the cause was here, but more importantly, would you treat this as DKA? We did, however, the ICU attending was adamant that this wasn’t DKA and shouldn’t be treated as such.
Thank You
NaHCO3 150 mEq stable in refridgerator for a week when mixed in a polyolefin/Excel/PAB bag.
Stability of sodium bicarbonate solutions in polyolefin bags.
Wear J, McPherson TB, Kolling WM.
Am J Health Syst Pharm. 2010 Jun 15;67(12):1026-9. doi: 10.2146/ajhp090301. Erratum in: Am J Health Syst Pharm. 2010 Oct 1;67(19):1586.
PMID:20516474
Extended Stability of Sodium Bicarbonate Infusions Prepared in Polyolefin Bags
AUTHOR(S)Sayre, Brian E.; Prettyman, Terrence; Kaushal, Gagan
SOURCEHospital Pharmacy;Jul2012, Vol. 47 Issue 7, p538
[…] episode Scott discusses the benefits of using Sodium Bicarb – Acid-Base VI – Chloride-Free Sodium and there are a […]
Hi Scott,
In the podcast you mention a magical concoction of insulin, dextrose, calcium, and bicarbonate used in a pediatric study to treat hyperkalemia – any chance you could post the reference? I’ve been looking for the article but can’t seem to find it. It sounds like a great way to treat hyperkalemic patients, especially if they make urine and you can give some lasix as well. I wanted to see what their recipe for the IV drip was to see if I could translate it to my adult patients. Thanks!
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