Sodium Bicarbonate

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JWebar

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Hey guys...
What do you think about the use of NaHCO3 in metabolic acidosis (in the OR)? Do you use it? When? How much? (per kg dose or based on BE)

May seem like a dumb question but this topic really troubles me...

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It's been discussed at length here but it's been a while. I'll give you my preferences but they are just that. I have partners that still use it but I never have been a fan, much less someone that uses it. I believe metabolic acidosis treatment is best handled by treating the root cause. I'm talking about in the OR specifically. I think BiCarb is even a worse treatment when used outside the OR since we are acutely aware of the timing we give it and make make the necessary adjustments to deal with the CO2 load. However, I was trained that the intracellular acidosis is the real issue with BiCarb and while we can blow off the CO2 we can't manage the intracellular or even worse possibly, the CSF
/CNS acidosis. I trained in a place that did lot of trauma and practiced in a place with lots as well. I have done so much trauma that I am completely at home with it. And I can count on one hand the number of times I've given BiCarb and I'll have fingers to spare. I have tried it when drips like epi or norepinephrine were not working and it isn't impressive. Fix the original cause is always best.

Now if you want to talk about THAM then it's a different story.
 
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That's when I use it. Things are circling the drain, they came in 90% dead and are losing ground, pH is in the basement and the carpenter is fashioning a box out in the hall.
I totally respect everything you post, IlD.
So let me ask you this, what are you treating here? What's the intracellular pH? I truly don't know, which is why I'm asking.
Personally, I have had many of these pts you describe and I haven't found BiCarb to make much difference. The only thing I have noticed to help was volume. And lots of it.
 
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I haven't used it since I was forced to in residency and am suspicious of the skills and knowledge of anyone that does.
 
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When the ph is 6.9-7.1 the heart doesn't pump so well. I get a lot of severely acidemic trauma patients and the standard resuscitation is PRBC/FFP/plts/bicarb/cacl.
 
When the ph is 6.9-7.1 the heart doesn't pump so well. I get a lot of severely acidemic trauma patients and the standard resuscitation is PRBC/FFP/plts/bicarb/cacl.
So why the BiCarb?
Is it knee jerk?
Is it how you were trained?

How does the BiCarb make the heart pump better?
 
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Personally, I think people use BiCarb to make their pts look better just before dropping them off in the ICU. BUT THIS IS THE WORST POSSIBLE TIME TO GIVE IT.
 
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That's when I use it. Things are circling the drain, they came in 90% dead and are losing ground, pH is in the basement and the carpenter is fashioning a box out in the hall.

Just cuz it's the Anesthesia SDN forum... we need to highlight ILD's excellent post!
 
Just cuz it's the Anesthesia SDN forum... we need to highlight ILD's excellent post!
Yeah that was excellent for sure.
I agree, when the box is being fashioned in the hall, then BiCarb might as well be given as long as we understand that the game is over already.
 
So why the BiCarb?
Is it knee jerk?
Is it how you were trained?

How does the BiCarb make the heart pump better?

Yes that's how we trained with trauma and liver transplants. I give it early and they have more stable hemodynamics and prettier blood gases. I've seen bicarb raise the blood pressure in hypotensive severely acidemic patients. Maybe by improving pH which improves the function of cardiac myocytes.

http://m.rsta.royalsocietypublishing.org/content/364/1842/1171.full.pdf
 
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I'll use it in kids who have gotten a big contrast load for a long cardiac catheterization and have developed a significant deficit in spite of hydration. I've also used it with good success in pulmonary hypertensive crises. In these situations I usually end up using 1-2 mEq/kg total.

Otherwise, yeah, really only when they're circling the drain.
 
Give it when the pH is <7.1-7.2 cause epi/vaso/what have you won't work when the pt is so acidemic. I've never heard of it being used to "make the heart pump better", just to make drugs that make the heart pump better work.
 
Give it when the pH is <7.1-7.2 cause epi/vaso/what have you won't work when the pt is so acidemic. I've never heard of it being used to "make the heart pump better", just to make drugs that make the heart pump better work.

Sorry, that's partly what I meant. You said it much better than me. I'm a foreigner. English is not my first language.;)
 
I totally respect everything you post, IlD.
So let me ask you this, what are you treating here? What's the intracellular pH? I truly don't know, which is why I'm asking.
Personally, I have had many of these pts you describe and I haven't found BiCarb to make much difference. The only thing I have noticed to help was volume. And lots of it.
As I implied, I give it when they have been resuscitated adequately with fluids/products, Ca is ok, and they are refractory to pressors and actively trying to die. Fortunately, even though at a L1 trauma center, this is uncommon for me. I have seen a couple patients improve after 1/kg of bicarb when they were still extremely acidotic (<7). Was it all fluid, would it have happened if I waited 5 more minutes? Perhaps, but when nothing else is working and you're pressure is from Epi blouses +/- cpr, that's pretty much all that's left to try.
 
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Agree with what has been said above.

Those that think that any acidemia itself is some bad thing to be routinely corrected, I see as inferior physicians. These folks usually don't bat an eye at significant alkalosis, which actually is potentially harmful from an oxygen offloading perspective.

Ironically, it's often these same folks who *induce* acidosis with indiscriminate NS. Drives me f'ing crazy when I see a chloride of say 112 and that the pt has been getting bicarb.

Anyway, yeah. Don't give bicarb unless you're throwing Hail Mary's to the just-about-dead. It doesn't help and can hurt.
 
I only use bicarb when pH is < 7.1 and they are unstable and I think improving their pH will improve the function of vasopressors I'm giving. Otherwise just work on fixing the cause of the acidemia.
 
Agree with what has been said above.

Those that think that any acidemia itself is some bad thing to be routinely corrected, I see as inferior physicians. These folks usually don't bat an eye at significant alkalosis, which actually is potentially harmful from an oxygen offloading perspective.

Ironically, it's often these same folks who *induce* acidosis with indiscriminate NS. Drives me f'ing crazy when I see a chloride of say 112 and that the pt has been getting bicarb.

Anyway, yeah. Don't give bicarb unless you're throwing Hail Mary's to the just-about-dead. It doesn't help and can hurt.

I think this post summarizes perfectly what I've been reading about bicarb use in the OR.
 
As I implied, I give it when they have been resuscitated adequately with fluids/products, Ca is ok, and they are refractory to pressors and actively trying to die. Fortunately, even though at a L1 trauma center, this is uncommon for me. I have seen a couple patients improve after 1/kg of bicarb when they were still extremely acidotic (<7). Was it all fluid, would it have happened if I waited 5 more minutes? Perhaps, but when nothing else is working and you're pressure is from Epi blouses +/- cpr, that's pretty much all that's left to try.
Seems like legitimate use of BiCarb. Right up until the cpr comment. I think if you are doing cpr then BiCarb is a poor choice. But I will agree that the damage is probably already done and you can't really make things much worse.

Wasn't BiCarb removed from ACLS a few years back.
 
I hardly ever use bicarb except as highlighted in the above posts. However, with CPR, I really only use it (and rarely) for some of those marathon codes. If beyond 20 mins, I might throw in an amp of bicarb, for hyperkalemia and just as a Hail Mary. Otherwise I think bicarb does more harm than good.

In the ICU my resident started it overnight for a guy with bad sepsis and ARDS. I had him on 4 ml/kg tidal volumes, sedated and paralyzed, and proned. I left and his pco2 was 68 and pH 7.18. Resident started bicarb overnight and then I get a call that pco2 was 93 and pH 6.9. Why? The guy was "maxed" on his ventilation, so the resident essentially injected him with carbon dioxide. Backfired. So I hate the stuff.
 
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How should I manage metabolic acidosis?

Metabolic acidosis associated with haemorrhagic shock is a product of hypoperfusion. Although correction of metabolic acidosis requires restoration of organ perfusion, volume replacement may need to be deferred until haemorrhage has been controlled.This requirement has led to a search for adjunctive pharmacological treatments to offset the pathophysiological consequences of acidaemia on other organ systems, the coagulation system in particular. The traditional treatment for severe lactic acidosis in critical illness is sodium bicarbonate, but little rationale for its use and no evidence of its effectiveness in general, or in the trauma setting, is available.22 Administration ofsodium bicarbonate produces carbon dioxide, which can require large increases in minute volume to clear. In addition, sodium bicarbonate decreases ionised calcium concentrations by about 10%, which has deleterious effects on coagulation and cardiacand vascular contractility.22 Tris(hydroxymethyl)aminomethane is a biologically inert amino alcohol capable of accepting hydrogen ions.23 Clinical experience with this product in trauma patients is limited and the precise role of tris(hydroxymethyl)aminomethane in trauma resuscitation is yet to be defined, although the possible applications are attractive in theory.

http://www.expeditionmedicine.co.uk/index.php/advice/resource/r-0032.html
 
How should I manage metabolic acidosis?

Metabolic acidosis associated with haemorrhagic shock is a product of hypoperfusion. Although correction of metabolic acidosis requires restoration of organ perfusion, volume replacement may need to be deferred until haemorrhage has been controlled.This requirement has led to a search for adjunctive pharmacological treatments to offset the pathophysiological consequences of acidaemia on other organ systems, the coagulation system in particular. The traditional treatment for severe lactic acidosis in critical illness is sodium bicarbonate, but little rationale for its use and no evidence of its effectiveness in general, or in the trauma setting, is available.22 Administration ofsodium bicarbonate produces carbon dioxide, which can require large increases in minute volume to clear. In addition, sodium bicarbonate decreases ionised calcium concentrations by about 10%, which has deleterious effects on coagulation and cardiacand vascular contractility.22 Tris(hydroxymethyl)aminomethane is a biologically inert amino alcohol capable of accepting hydrogen ions.23 Clinical experience with this product in trauma patients is limited and the precise role of tris(hydroxymethyl)aminomethane in trauma resuscitation is yet to be defined, although the possible applications are attractive in theory.

http://www.expeditionmedicine.co.uk/index.php/advice/resource/r-0032.html

Tris(hydroxymethyl)aminomethane, Otherwise known as THAM.
Anyone else out there using this?
I have many times and it is beneficial. Impressively.
My residency was a large trauma center. I used this stuff often there.
 
I hardly ever use bicarb except as highlighted in the above posts. However, with CPR, I really only use it (and rarely) for some of those marathon codes. If beyond 20 mins, I might throw in an amp of bicarb, for hyperkalemia and just as a Hail Mary. Otherwise I think bicarb does more harm than good.

In the ICU my resident started it overnight for a guy with bad sepsis and ARDS. I had him on 4 ml/kg tidal volumes, sedated and paralyzed, and proned. I left and his pco2 was 68 and pH 7.18. Resident started bicarb overnight and then I get a call that pco2 was 93 and pH 6.9. Why? The guy was "maxed" on his ventilation, so the resident essentially injected him with carbon dioxide. Backfired. So I hate the stuff.

But in the operating room, we can and do easily blow off the co2. We've all seen the transient rise in etco2 when we give bicarb and we've all seen it go away in a matter of minutes.
 
But in the operating room, we can and do easily blow off the co2. We've all seen the transient rise in etco2 when we give bicarb and we've all seen it go away in a matter of minutes.

Yup, agreed. But for that ARDS patient, I already had him on "max" ventilation. With tidal volumes of 4 ml/kg, he required a high RR to clear co2. IIRC, I was using tidal volumes of 380 at a rate of 35 for him, giving me a minute ventilation of 13.3 L/min (plus some auto-peep but nothing major). It's not too high a MV, due to the extremely low tidal volumes, but at that RR, I couldn't really provide more minute ventilation to clear the co2 provided by the bicarb infusion, hence the paradoxical worsening of acidemia. That's the point I wanted to pass on to my resident because I've had traumas in residency where I was basically doing the same thing for acidosis.

Besides, my fellowship ICU doesn't use etco2 yet; it's on its way. But I don't think it correlates with paco2 as well in the unit.
 
Tris(hydroxymethyl)aminomethane, Otherwise known as THAM.
Anyone else out there using this?
I have many times and it is beneficial. Impressively.
My residency was a large trauma center. I used this stuff often there.

I used THAM once in the unit in my fellowship for a patient who was still on ECLS but having difficulty ventilating when the sweeps were off. I wanted to see if I could buffer his pH (which would fall to 7.1) and get him off ECLS, which was a major source of hemorrhage. Never had it in residency where I did a lot of trauma. My new anesthesiology/CCM job doesn't officially start until end of next month, and I won't do trauma anymore. But hey, I may consider it.
 
Last month took an old lady from the MICU POD 4-5 s/p a complicated open chole with a hepatic artery injury to the OR for hemorrhagic shock, suspected bleeding from the hepatic artery as abdomen was tight, tense, and actively oozing blood from the old incision. On max neo, vaso, norepi, and we set up epi just prior to transport. pH 6.9ish to start, once they opened the epi was titrated up and after ~10 units pRBCs, 10 FFP, platelets, and cryo over the next hour or so while they dealt with the arterial bleed she basically only responded to boluses of Ca and epi. We ended up giving bicarb a couple times to try and help our pressors a bit, but the carpenter had the polish out so at that point it didn't matter.

Anyhow, somehow she survived the OR and my buddy up in the SICU had THAM in his hand ready to go once I brought her back up. I had been randomly updating him on the ABGs/transfusion status as he knew he was inheriting a mes. It was the first time I had seen it at our institution but in the last few weeks since then I've seen it used in a number of SICU patients.

Oh, and she died 3 days later. But survived the OR!

Fun times, great thread as well. Appreciate the folks who contribute.
 
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