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

[display-posts tag=”acid-base-3″]

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 gas

For 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 mmHg

However 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

Editor-in-Chief, EMCrit.org at EDECMO LLC

An ED Intensivist from NY. No conflicts of interest (coi).

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