DKA + Hyper K, ? Bicarb

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docB

docB

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It seems like in Vegas all the DKA has some degree of renal failure and hyperkalemia as opposed to the classic normal to low K that you have to monitor for decreases as the insulin drives the K intracellular. I've got a guy right now with a glucose of 900, Bicarb of 11, gap of 34, K of 6.7 and EKG changes in the form of peaked Ts.

So do you give this guy Bicarb? The bicarb would help with the hyperkalemia which despite being only 6.7 is causing EKG changes. But bicarb in the setting of DKA can lead to cerebral edema.

So what to do?

The acetone and ABG are pending and NS, insulin gtt, kayexelate, Ca and albuterol are all running. More later. Code (not this guy)!
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I would just stick with Insulin and NS for now, and and do bicard if pH goes <7.0
 
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Also, how many slurpee's does it take to get your bood glucose to 900?
gawd Dam!
 
Repeat met panel shows improvement: Na 131, K 5.3, Cl 90, Bicarb 12, glu 642, BUN 36 and Cr 1.8. Glu had plummeted so I had to dial back the gtt then it shot up again.

So it seems holding the bicarb was the right decision. I hear you guys about holding off unless the pH is below 7 but what about the hyperkalemia issue. This guy had EKG changes but they were minor. What if you've got a guy with a K of 7.5 and QRS widening. Bicarb then? Save the heart and deal with the possibility of cerebral edema later?
 
It's been a while since I've managed DKA (in the PICU), but it's fun mental masturbation.
Does his coexisting metabolic alkalosis make any difference in your choice?
 
I thought I read somewhere that cerebral edema with bicarb was more predominant in the pediatric population. I probably would have rechecked labs after 2L NS and the drip and held off the bicarb as well... although with EKG changes, that's a tricky call. Sounds like you did everything else in the hyperK protocols, though.
 
By the way the above question is an esoteric acid-base based question so feel free to ignore; I was just curious.

I wonder if keeping the insulin going (as well as other hyper K drugs) and upping fluid dextrose for hypoglycemia avoidance might allow for effective tx without the bicarb. If not, ultimately it's a tough choice but fatal arrhythmia will kill fast; you may get away with txing the [potential] cerebral edema later.

Interesting question to posit.
 
In a patient with a critical hyper K I would give the bicarb and bicarb gtt even with the concomitant metabolic alkalosis in an attempt to drive more K intracellular.

The big paper on the DKA+bicarb=cerebral edema was done in peds. However it was predominantly Type 1 diabetics in their mid to late teens so physiologically adults. That was the paper in NEJM. Nate Kupperman is one of the PIs for that and it came out in 2002 (I think) so everyone in my residency was well aware of it.
 
Insulin and IVF will probably do enough to correct the acidemia and hyperK. I wouldn't give bicarb to this guy because the K is going to drop with the treatment you're giving and as you mention, it's associated (though I don't think proven causal) in cerebral edema.

I was taught to only use bicarb in DKA patients in cardiovascular collapse, which is fairly uncommon.
 
Hawkeye Kid said:
Insulin and IVF will probably do enough to correct the acidemia and hyperK. I wouldn't give bicarb to this guy because the K is going to drop with the treatment you're giving and as you mention, it's associated (though I don't think proven causal) in cerebral edema.

I was taught to only use bicarb in DKA patients in cardiovascular collapse, which is fairly uncommon.
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I agree. I also agree with adding a little sugar to the fluids if the glucose drops too fast and you need the insulin to treat the hyperK.

Also, don't forget about albuterol for hyperK. I've given it once for hyperK (10.1!, in addition to everything else on the K list). I don't know that I'd give it in this case, given the relatively mild EKG changes,
 
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docB said:
In a patient with a critical hyper K I would give the bicarb and bicarb gtt even with the concomitant metabolic alkalosis in an attempt to drive more K intracellular.

The big paper on the DKA+bicarb=cerebral edema was done in peds. However it was predominantly Type 1 diabetics in their mid to late teens so physiologically adults. That was the paper in NEJM. Nate Kupperman is one of the PIs for that and it came out in 2002 (I think) so everyone in my residency was well aware of it.
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http://content.nejm.org/cgi/content/abstract/344/4/264
 
docB said:
This guy had EKG changes but they were minor. What if you've got a guy with a K of 7.5 and QRS widening. Bicarb then? Save the heart and deal with the possibility of cerebral edema later?
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since you've already got the Ca, the albuterol and insulin, hammer him with more albuterol and throw in lines for possible emergent dialysis if you're really worried about it. But don't forget the importance of fluid resuscitation in a hyperkalemic pt as a modality for treating hyperK in DKA. I wouldn't use bicarb unless they get to the widened QRS changes on EKG and frankly, I don't use bicarb even if the pH is less than 7.0 with the exception that I once had a DKA pt who was also on pressers and barely responding to them, the bicarb helped the BP.
 
Interesting discussion. So it sounds like the consensus is trending toward no bicarb unless the pH is <7 or there are signs of circulatory collapse. Remember that we're talking about DKA with hyper K here and when you have to pull the trigger to treat the K. Does anyone use bicarb routinely for DKA alone, ie. with a K that is normal or mildly elevated without EKG changes?
 
Measured Bicarb 11 and ABG 7.16/26/79?

May seem a bit esoteric but these numbers, by Winter's Formula, calculate out to a well compensated metabolic acidosis, yet the pH is 7.16?:rolleyes:

Was this an ABG or VBG?

If ABG there may be a problem with the numbers, not sure they are internally consistent, or serum bicarb dropped significantly between blood sample from panel and arterial blood sample.

If serum bicarb dropped significantly between samples it looks like the patient would benefit from BiPAP or Intubation/mechanical ventilation as he would then also have a respiratory acidosis. I wouldn't consider bicarb administration in combined metabolic and respiratory acidosis before driving up minute ventilation.
 
Phlegm said:
Measured Bicarb 11 and ABG 7.16/26/79?

May seem a bit esoteric but these numbers, by Winter's Formula, calculate out to a well compensated metabolic acidosis, yet the pH is 7.16?:rolleyes:

Was this an ABG or VBG?

If ABG there may be a problem with the numbers, not sure they are internally consistent, or serum bicarb dropped significantly between blood sample from panel and arterial blood sample.

If serum bicarb dropped significantly between samples it looks like the patient would benefit from BiPAP or Intubation/mechanical ventilation as he would then also have a respiratory acidosis. I wouldn't consider bicarb administration in combined metabolic and respiratory acidosis before driving up minute ventilation.
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This isn't esoteric at all, I use winter's almost daily, granted i'm not EM. But I think you're missing a key point with the Winter's equation. The body will never be able to fully compensate for an acidemia this severe, the winter's merely predicts that the appropriate resp compensation is going to be. So yes, it is not surprising to see a low pH with an appropriately predicted CO2 per winters, so this is a appropriate respiratory response and falls inline with my own personal observations of ph/HCO3 in DKA pts. I guess more to the point, winter's merely predicts body's appropriate response to lower the CO2 in the setting of a metabolic acidosis, not how low it has to drop the CO2 to normalize the pH

As far as bipap/Venting, you're going to have a time with blowing down the CO2 much more.

From the PCO2 equation [(PCO2 = (VCO2 x 0.863)/MV] assuming a low presentation MV of 10L/min with the above gas, you'll have to increase MV to 15L/min to get the CO2 down to 18, and 20L/min to get t a CO2 of 13. Now if he's actually working when he came in with a MV of 15L/min then you would then have to increase MV to 20L/min to get a CO2 of 19.5 or a 25l/min to get a CO2 of 16. which of course would be 1000mL TV at a rate of 25 or a TV of 500 at a rate of 50. Which means that you're going to be using TV that is much larger than I'd like to use in most pts unless they're 8 foot tall or using a ridiculously high RR. And even then, those ridiculously high MV's aren't going to have that much of an affect on the pH
 
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Hernandez said:
This isn't esoteric at all, I use winter's almost daily, granted i'm not EM. But I think you're missing a key point with the Winter's equation. The body will never be able to fully compensate for an acidemia this severe, the winter's merely predicts that the appropriate resp compensation is going to be. So yes, it is not surprising to see a low pH with an appropriately predicted CO2 per winters, so this is a appropriate respiratory response and falls inline with my own personal observations of ph/HCO3 in DKA pts. I guess more to the point, winter's merely predicts body's appropriate response to lower the CO2 in the setting of a metabolic acidosis, not how low it has to drop the CO2 to normalize the pH

As far as bipap/Venting, you're going to have a time with blowing down the CO2 much more.

From the PCO2 equation [(PCO2 = (VCO2 x 0.863)/MV] assuming a low presentation MV of 10L/min with the above gas, you'll have to increase MV to 15L/min to get the CO2 down to 18, and 20L/min to get t a CO2 of 13. Now if he's actually working when he came in with a MV of 15L/min then you would then have to increase MV to 20L/min to get a CO2 of 19.5 or a 25l/min to get a CO2 of 16. which of course would be 1000mL TV at a rate of 25 or a TV of 500 at a rate of 50. Which means that you're going to be using TV that is much larger than I'd like to use in most pts unless they're 8 foot tall or using a ridiculously high RR. And even then, those ridiculously high MV's aren't going to have that much of an affect on the pH
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Reply appreciated.
I continue to question the internal consistency of the ABG results posted by the OP. The calculated bicarb (omitted in the question if an ABG) would be between 8 and 9 suggesting inadequate respiratory compensation/relative respiratory acidosis. I frequently treat patients with severe DKA, some requiring vent support, in the ICU. I am just as aware that Winter's represents maximal compensation (at 12-24 hours) as I'm sure you are aware that its usefulness is minimal in processes that have been ongoing less than 12-24 hours since you use it almost daily. The OP's question was regarding whether or not bicarb administration was warranted in the setting he outlined. I say no, maybe you say yes as you suggest little benefit from mechanical ventilation which I disagree with in the setting of hyperkalemia. There are clearly providers who are more enthusiastic about bicarb use than I am in settings of DKA and lactic acidosis. In my opinion a hemodynamically stable patient, with DKA and pH 7.16, and relative respiratory acidosis may need need ventilatory support (BiPAP or tube) rather than a bicarb drip. Are you arguing for the bicarb drip?
 
Phlegm said:
Reply appreciated.
I continue to question the internal consistency of the ABG results posted by the OP. The calculated bicarb (omitted in the question if an ABG) would be between 8 and 9 suggesting inadequate respiratory compensation/relative respiratory acidosis.
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The internal consistency of the ABG is fine. The Kassirer-Bleich equation puts the hydrogen concentration between 58-79 (depending on if you use measured or calculated which I use calc'd for these purposes) which translates to a pH between 7.12-7.22. I get 8.9 for a calc'd bicarb. Personally, I wouldn't quible about a CO2 of 26 when the predicted CO2 off of a calc'd bicarb is 23.5 in a pt who's showing now respiratory distress. so personally this isn't a severe enough resp acidosis unless he's showing signs of tiring out.

Phlegm said:
The OP's question was regarding whether or not bicarb administration was warranted in the setting he outlined. I say no, maybe you say yes as you suggest little benefit from mechanical ventilation which I disagree with in the setting of hyperkalemia. There are clearly providers who are more enthusiastic about bicarb use than I am in settings of DKA and lactic acidosis. In my opinion a hemodynamically stable patient, with DKA and pH 7.16, and relative respiratory acidosis may need need ventilatory support (BiPAP or tube) rather than a bicarb drip. Are you arguing for the bicarb drip?
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See above but I almost never use bicarb in DKA as I've stated before. I also would not use MV unless they were showing signs of respiratory distress, and in the setting of EKG changes, I'd press the nephrologist to dialysis as bicarb/albuterol/insulin are merely temporizing measures anyways, kayexalate and diaylsis are definitive. My perspective on the MV is that it isn't a benign treatment, and unless they need it for resp failure or airway protection, I avoid it, now if this guy starts tiring out, then absolutely, but without a clinical indication that he's failing, I would not intubate and even if he was I'd more than likely start with NIPPV.

But as I alluded to earlier, in a DKA pt, volume replacement is an effective means of treating hyperkalemia most of the time due to the severe level of dehydration and total body potassium depletion is amenable to IVF.

ETA: although you do make an interesting point about using MV to help with the acidosis to treat the hyperK, I went back and reran the numbers and you're decreasing the CO2 from 26 to 20 will lead to an increase in pH to 7.28, which equates to increasing the MV by 5L/min so depending on where they're starting from, that might not be that hard to do, but if you're already starting with a high MV, then it's going to be hard to make that increase.
 
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just a lowly pharmacy resident here - but why wouldn't changing the IVF to D5/NS or even D10/NS along with increasing the rate of the insulin gtt work?

The hyperkalemia should resolve with hydration, correction of the acidosis and the presence of insulin right?
 
docB said:
It seems like in Vegas all the DKA has some degree of renal failure and hyperkalemia as opposed to the classic normal to low K that you have to monitor for decreases as the insulin drives the K intracellular. I've got a guy right now with a glucose of 900, Bicarb of 11, gap of 34, K of 6.7 and EKG changes in the form of peaked Ts.

So do you give this guy Bicarb? The bicarb would help with the hyperkalemia which despite being only 6.7 is causing EKG changes. But bicarb in the setting of DKA can lead to cerebral edema.

So what to do?

The acetone and ABG are pending and NS, insulin gtt, kayexelate, Ca and albuterol are all running. More later. Code (not this guy)!
Click to expand...

docB said:
Repeat met panel shows improvement: Na 131, K 5.3, Cl 90, Bicarb 12, glu 642, BUN 36 and Cr 1.8. Glu had plummeted so I had to dial back the gtt then it shot up again.

So it seems holding the bicarb was the right decision. I hear you guys about holding off unless the pH is below 7 but what about the hyperkalemia issue. This guy had EKG changes but they were minor. What if you've got a guy with a K of 7.5 and QRS widening. Bicarb then? Save the heart and deal with the possibility of cerebral edema later?
Click to expand...

J-Rad said:
By the way the above question is an esoteric acid-base based question so feel free to ignore; I was just curious.

I wonder if keeping the insulin going (as well as other hyper K drugs) and upping fluid dextrose for hypoglycemia avoidance might allow for effective tx without the bicarb. If not, ultimately it's a tough choice but fatal arrhythmia will kill fast; you may get away with txing the [potential] cerebral edema later.

Interesting question to posit.
Click to expand...

My post will essentially agree with what the other posters have said. Putting on my med-peds hat (and my experiences with treating DKA in medicine patients as well as pediatrics patients) ...

I would have held off on bicarb as well. Bicarb in the setting of metabolic acidosis and hyperkalemia has a really unpredictable response (to hyperkalemia), especially if your patient is a chronic renal patient (dunno what your patient's baseline Cr is, and whether the Cr of 1.8 is all pre-renal or not)

I probably would have held off on kayexalate, since it's not an immediate solution for hyperkalemia and you don't want it kicking in when you start dealing with hypokalemia (or trying to prevent hypokalemia). Hopefully the calcium bought you some time to get the bolus in and the insulin started. Once the effect of calcium starts to wear off after several hours, hopefully the potassium is lower that you are no longer seeing cardiac toxicity

As for the glucose dropping too quickly, since the gap went from 34 to 29 (and the bicarb stayed essentially the same), I would have kept the insulin drip at exactly the same rate and started dextrose infusion (and the reason why I like the Y-tubing used in peds - you can hang a bag of D10-1/2NSS via pump and another bag of 1/2NSS via another pump and control the rate of both so you can control how much %dextrose is going in). You keep the total infusion rate the same but control how much of each bag is going (ie if the total rate is 250ml/hr, you can do 100/hr of the dextrose and 150/hr of the saline) ... and adjust the rates of each accordingly based on the hourly accuchecks


If I start seeing QRS widening associated with hyperkalemia and DKA - it's time to throw in a dialysis catheter and call nephrology for possible emergent dialysis. Of course this too takes time so bicarb might be appropriate in this setting (along with expert consultation)

in summary - basically I agree with the above posters :D
 
group_theory said:
I probably would have held off on kayexalate, since it's not an immediate solution for hyperkalemia and you don't want it kicking in when you start dealing with hypokalemia (or trying to prevent hypokalemia).
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Yes, giving Kayexalate would be the exact wrong thing to do for a DKA patient. It's important to remember that, while their initial serum K may be high, normal, or low, all of these patients have a low total body K. Doing anything to lower their overall K is just going to cause you to play catch up later as the insulin and IVF lower their serum K. I suppose the exception to this might be the ESRD patient with DKA since they wouldn't lose K in their urine, but I've never seen it.
 
Had one last week. Glucose 1500, K was 6.8. Initially he only had peaked T-waves, but then he went into cardiac arrest. After running ACLS for about 10 minutes, I think the 2nd amp of bicarb was what brought him back. He lives to suck more resources out of society (BTW he was IVDA and non-compliant).
 
So to answer several of the above posters:

The initial bicarb was from the basic met panel which was drawn soon after presentation, ie. before any therapy. The ABG was done ~2.5 hours in after the initial met panel came back. At that point the pt had had >2L of NS.

I gave the kayexelate because I was faced with a hyperkalemic patient with EKG changes. At that point DKA was on the differential but so was acute renal failure due to dehydration in a diabetic with CRI. I was less worried about having to play catch up down the line than with trying to reduce the cardiac toxicity. Giving the kayexelate or not is certainly a reasonable thing to debate but it's one of those decisions that gets made based on incomplete info. Of note in Vegas I have about as much chance of getting a dialysis catheter into someone and getting emergent dialysis as I do of getting a plastics or ENT consult.

Switching to D10NS and keeping the insulin gtt going at the same rate would work. In my hospital D10NS has to come from pharmacy (we don't have it in the ED) so that takes about an hours to get going (write the order, fax the order, verify the order, send a tech, get the bag, find a pump, hang the bag, etc.). Given the worry about the glu dropping too much I reduced the gtt for the time being.
 
docB--My comment about Kayexalate was meant to address treating hyperkalemia in a pt with known DKA, not to suggest that you were a ***** for giving it to this guy. Sorry if it came across differently.
 
Hawkeye Kid said:
docB--My comment about Kayexalate was meant to address treating hyperkalemia in a pt with known DKA, not to suggest that you were a ***** for giving it to this guy. Sorry if it came across differently.
Click to expand...

No no. No offense taken. I think this is a great discussion and as a community guy it's as close as I get to M&M any more. I also think it's always a good idea to step back and take a look at the way you deal with the commonplace disease processes we see. It's easy to get complacent.

I mainly chimed back in to explain the chronology of the results I was getting and explain some of the diagnostic uncertainty I had and some of the systems limitations I was up against.

As for the Kayexelate I probably would have given it again in this guy given the circumstances and data I had at that moment. But I think I might have given it reflexively in a known DKAer with hyperK before thinking about it to this degree.
 
docB said:
Switching to D10NS and keeping the insulin gtt going at the same rate would work. In my hospital D10NS has to come from pharmacy (we don't have it in the ED) so that takes about an hours to get going (write the order, fax the order, verify the order, send a tech, get the bag, find a pump, hang the bag, etc.). Given the worry about the glu dropping too much I reduced the gtt for the time being.
Click to expand...

This alone motivates me to interview with community hospitals too. That's effing ridiculous.
 
I work at a community hospital in Vegas. I've never had a problem yet getting a dialysis cath placed, or a nephrologist to see the patient.

If it's really emergent, can place a dialysis cath myself in the ER. I've done 2-3 this year.
 
I can get nephro to order dialysis if it's one of their group's established patients. Otherwise it gets a little tricky and we don't have nephrology on call. I've put in 2 dialysis caths since I've been here but I really don't like to do it. The risk of complications goes up as you shove bigger and bigger things in there. We usually temporize as well as we can and then the admitting doc tries to get a vasc surgeon to do the cath. Rads can do them too if they have an IR crew available.
 
docB said:
I can get nephro to order dialysis if it's one of their group's established patients. Otherwise it gets a little tricky and we don't have nephrology on call. I've put in 2 dialysis caths since I've been here but I really don't like to do it. The risk of complications goes up as you shove bigger and bigger things in there. We usually temporize as well as we can and then the admitting doc tries to get a vasc surgeon to do the cath. Rads can do them too if they have an IR crew available.
Click to expand...

I usually talk to the admitting doctor and find out what renal physician they want me to call. So far I've never had one refuse to start dialysis on an inpatient when requested.

99% of the time I have IR place the caths under fluoro.
 
Wow. I think this might be a first. A thread jacking by, what I'm guessing, are some sort of medicine fellows. Not that I mind, I found the discussion very interesting. Thanks for jumping in.

DocB, I probably wouldn't have given bicarb. Not for any great scientific rationale but because it just isn't my usual practice. I usually just give Ca and then pound way with fluids, insulin and albuterol.

I probably would have held on the kayexelate, too. That, of course, assumes I knew it was DKA as the etiology up front. It sounds like this wasn't clear at the time so who knows what I would have done.

Thanks for starting up an interesting discussion, though.

Take care,
Jeff
 
Jeff698 said:
Wow. I think this might be a first. A thread jacking by, what I'm guessing, are some sort of medicine fellows.
Click to expand...

You knew it couldn't be the IM guys because no one mentioned checking a phosphorous. If we start talking about phos then you know the medicine pod people have taken over and we're in flea land.
 
docB said:
You knew it couldn't be the IM guys because no one mentioned checking a phosphorous. If we start talking about phos then you know the medicine pod people have taken over and we're in flea land.
Click to expand...

That's only if the renal fellows or the BMT folks get involved. Nobody else cares about the Phos.
 
I can't read all of these because I am 14 hours into my 16 hour day and the ED is seriously constipated with my waiting room filling up.

But here would be my take: IVF (several liters, quickly), potentially NO insulin (would give several liters first), maybe kayexolate for hyperK but probably not. but maybe.

No bicarb. pretty much ever in DKA. hasn't been shown to do much other than make us as the physician feel better.


anywho. I'll try and explain more later.
 
docb, i think you did it right.


docB said:
You knew it couldn't be the IM guys because no one mentioned checking a phosphorous. If we start talking about phos then you know the medicine pod people have taken over and we're in flea land.
Click to expand...

i'd check the phos, as well as a magnesium on my own later. :p
 
roja said:
But here would be my take: IVF (several liters, quickly), potentially NO insulin (would give several liters first), maybe kayexolate for hyperK but probably not. but maybe.

No bicarb. pretty much ever in DKA. hasn't been shown to do much other than make us as the physician feel better..
Click to expand...

Really? No insulin?
 
docB said:
It seems like in Vegas all the DKA has some degree of renal failure and hyperkalemia as opposed to the classic normal to low K that you have to monitor for decreases as the insulin drives the K intracellular. I've got a guy right now with a glucose of 900, Bicarb of 11, gap of 34, K of 6.7 and EKG changes in the form of peaked Ts.

So do you give this guy Bicarb? The bicarb would help with the hyperkalemia which despite being only 6.7 is causing EKG changes. But bicarb in the setting of DKA can lead to cerebral edema.

So what to do?

The acetone and ABG are pending and NS, insulin gtt, kayexelate, Ca and albuterol are all running. More later. Code (not this guy)!
Click to expand...

Pretty good discussion for SDN.

1. With DKA you HAVE to give insulin given that the reason for the electrolyte aberrations are due to a lack of insulin. For HHNK, where osmolality is more the cause, the fluids become much more critical than the insulin.

2. I've seen plenty of people "compensating" with a pH in the 7.17 range with DKA. They will turn around quickly with insulin and fluids. I wouldn't BiPaP them. I would convert the ketoacids back while keeping a close eye on whether or not they're tired. If they have concominant pulmonary disease, DKA can tip 'em over quickly.

3. For the hyperkalemia THE most important will be the fluids and insulin. You can give calcium chloride/carbonate for "membrane stabilization" if the ECG is freaking you out - but you should expect the K+ to respond quickly to NS and insulin. This guy was almost assuredly hyperK+ from intracellular shift BUT total K+ deplete from urinary losses in the setting of an osmotic diuresis. I would not have given kayexylate unless the K+ didn't budge with NS/insulin as that would make me think that maybe renal failure is playing into this more than I had anticipated.

4. Watch that phosphorus - with someone exhibiting compensatory tachypnea you need to make sure that they have the phos to keep that required energy available. Low phos can cause respiratory arrest.

5. Bicarb - I give it if there are no electrolyte abnormalities in someone with a nongap acidosis AND I give it when I have refractory hypotension in the setting of pressures and a severe gap acidosis pH < 7.1'ish (overwhelmingly from lactate). There are a couple papers out of U of Chi that actually make the case for bicarb worsening intracellular pH while improving extracellular pH. I've never seen Bicarb turn around someone with multiorgran failure on pressors..I have seen it help for someone who has true bicarb loss (nongap).
 
I'm an EM resident (not a medicine guy...sorry), and I work in an ED which breaks a great majority of DKA's in-house due to a limitation on ICU beds, plus some of the critical care attendings work in the ED as well. It's funny that I should find this thread as we just had a discussion on bicarb in acidosis this morning on ICU rounds.

I have to agree with Soulja on this one. The insulin and correction of the acidosis should drive the extracellular K (which is where the lab reading is coming from) back into the cell and should do so very rapidly. Bicarb is basically seen as a no-no mostly because of the worsening of intracellular pH, but also that there's little data to back it's use.

My question for everyone is what do most of you use for fluid choice? We use Normosol/plasmalyte exclusively. NS is hyperchloremic and may serve to worsen acidosis. Additionally the fluids pH is ~5.5 (vs. 7.4 of normosol).

Anyway, great question and discussion.
 
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