Pushing Bicarb Pre-intubation

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Howdy all -

Have a question for the smarter ones than me on here regarding acidosis & bicarb...

In the setting of metabolic acidosis (severe sepsis, salicylates, etc) with pH ~7 or lower, I know typically a bicarb drip gets started (especially for salicylate poisoning)... however, when these patients need to be intubated, there's a few potential problems:

1) we can't possibly replace their own respiratory rate/compensation
2) sometimes they get paralyzed, and at least get sedated

The net result of these is a potential increase in respiratory acidosis during the peri-intubation period (yea, several case reports discuss the complications of intubating a salicylate-poisoned patient). As such, I've begun recommending pushing 1-2 amps of NaHCO3 immediately before intubation, as an adjunct to RSI.

However, I only do this based on my understanding of the underlying pathophys & acid/base, as well as the pharmacokinetics of ASA (and subsequently derive it over into any significant metabolic acidosis that needs to be intubated). I can't find a good reference in the literature to back this up otherwise.

Anyone out there have any useful citations regarding this?

Appreciate the input...

-t

There really isn't a lot of data that shows pushing bicarb amps for any condition is helpful. We only do it because of the theoretical.

Just set them on a high rate/low TV vent, and don't waste time during intubation. The likelihood of sudden arrest because you pushed them over the limit with their acidosis is so rare that when it happens you get a paper out of it.

Kind of two different things though... The ASA toxicity gets the bicarb drip for urinary alkalinization, primarily, increasing the ASA excretion, but from everything I've read so far... using it in anything else is still voodoo (along with the metabolic acidosis from ASA). Sure, it raises the arterial pH, but the data doesn't seem to show that it has a commensurate effect on intracellular/tissue pH, then you've got the volume load, transient intracranial pressure increase, CO2 load from bicarb breakdown, the physiology just gets over my head but I can't seem to find any generalized consensus on the newest data that it's ever a good idea. It seems like we continue to do studies using bicarb on metabolic acidosis and always come to the same conclusion... yet plenty of people still seems to use it to treat a number on an blood gas.

Do you use the bicarb for your non ASA toxicity pt's? What's your exact rationale out of curiosity? I think from the respiratory acidosis standpoint, you would quickly mitigate this with a quick tube and an element of hyperventilation. Most are getting hyperventilated as their being bagged in the first place getting ready for RSI which is more than likely causing a respiratory alkalosis. Are you arguing that you can alkalinize the urine more quickly for the ASA pts?

What is the most common situation that leads to you guys (EM docs) giving bicarb?

Any situations where from personal experience bicarb would be indicated but you try to avoid it for one reason or another?

I've never given it in the field, and only once during my ED rotations but I don't remember what for anymore....it seems to be one of those useless meds that could disappear from the drug box and not be missed

TCA overdoses with QRS widening

Amal Mattu recommended it on one of the EMRAPs (Mar 2010?) in the peri-intubation period as a strategy for lowering the risk of PEA secondary to acidosis of the few min between drugs, tube, vent set up, . . .

Originally Posted by Tiger26

Amal Mattu recommended it on one of the EMRAPs (Mar 2010?) in the peri-intubation period as a strategy for lowering the risk of PEA secondary to acidosis of the few min between drugs, tube, vent set up, . . .

Bicarb in general is not useful and can be in fact harmful in most metabolic acidosis settings.

There are only two situations where I think bicarb is useful:

1. TCA overdose

2. Hyperkalemia

Originally Posted by GeneralVeers

Bicarb in general is not useful and can be in fact harmful in most metabolic acidosis settings.

There are only two situations where I think bicarb is useful:

1. TCA overdose

2. Hyperkalemia

Yeah, but in TCA overdose it has nothing to do with the bicarb itself, just the sodium cation that is hypertonic. 3% saline will do the same, because you're trying to affect sodium channels, not acid/base status.

Originally Posted by Dr.McNinja

Yeah, but in TCA overdose it has nothing to do with the bicarb itself, just the sodium cation that is hypertonic. 3% saline will do the same, because you're trying to affect sodium channels, not acid/base status.

My understanding has always been 2 parts... the sodium channel part, of which there is a sodium dependent part and a pH dependent part, and then the goal of making the blood more alkaline which promotes release of TCA from albumin/protein binding. I thought that was always the rationale for bicarb...

Originally Posted by Dr.McNinja

Yeah, but in TCA overdose it has nothing to do with the bicarb itself, just the sodium cation that is hypertonic. 3% saline will do the same, because you're trying to affect sodium channels, not acid/base status.

Hmmm, grab the bicarb off the code cart, or enter computer order for 3% saline and drum fingers for an hour ...

Originally Posted by Groove

My understanding has always been 2 parts... the sodium channel part, of which there is a sodium dependent part and a pH dependent part, and then the goal of making the blood more alkaline which promotes release of TCA from albumin/protein binding. I thought that was always the rationale for bicarb...

Unbound TCA would be more toxic than bound. Not sure the theoretical is backed up there.

Originally Posted by Groove

My understanding has always been 2 parts... the sodium channel part, of which there is a sodium dependent part and a pH dependent part, and then the goal of making the blood more alkaline which promotes release of TCA from albumin/protein binding. I thought that was always the rationale for bicarb...

For TCAs it's more the sodium moiety, the bicarb part is secondary - Dr. McNinja's right about the hypertonic saline - and it's also why bicarb DRIPS don't work for TCAs, you need boluses.

As for the ASA and the above posters, indeed, the bicarb gtt enhances elimination; however, ASA patients who are progressing to the point of requiring intubation are already pretty sick - combination of hyperventilation 2/2 direct medullary stimulation as well as a need to blow off the metabolic acidosis... results in crump-tastic intubations if one is not very careful/lucky.

@Tiger26: yeah, I heard that way back when, but could never find a reference... it's all theoretical (thus my original post).

@Groove: I only use pre-intub bicarb for my ASA patients... but, I do everything in my power to NOT intubate the salicylates; any drop in pH increases the non-ionized ASA in the serum, which results in ASA in the brain, which results in badness. The time between intubation & hooking up the vent with appropriate settings can be minimized, but it's not zero. We can't match the patient's hyperpnea/tachypnea with mechanical ventilation, not to mention that ET diameter is invariably smaller than the pt's native trachea - so they'll generally run the risk of getting sicker in the setting of big ingestions.

My only thought was whether or not this peri-ventilatory period of relative respiratory hypoventilation and pH effects for non-ASA patients was amenable to bicarb - one of our ICU docs swears by it, and theoretically might be a good idea, but I've no lit to back his horse.

Thanks all for the help, btw; glad to know my PubMed/Google/Phrenology/Astrolabe skills weren't faulty and that there really aren't any references out there on this other than the occasional case report.

Cheers!
-t

Speaking to the original theory of giving bicarbonate as an adjunctive treatment during intubation in someone who is maintaining a respiratory alkalosis in response to their metabolic acidosis - I like the idea, but, medicine is littered with good ideas that turned out to be harmful.

In addition to TCA and other overdose situations with QRS widening, I give bicarbonate to seizing hyponatremic patients because the 3% is not as readily available.

Originally Posted by GeneralVeers

Bicarb in general is not useful and can be in fact harmful in most metabolic acidosis settings.

There are only two situations where I think bicarb is useful:

1. TCA overdose

2. Hyperkalemia

Disclaimer: The following may not be helpful to ED physicians.

I have found bicarb to be incredibly helpful when patients are very acidotic, hemorrhaging and circling the drain. With the administration of bicarb in a dire situation I have seen patients perk up immediately, CO2, BP, pulse ox and HR. Of course this is a temp fix that may allow pressors to work better as well.

My understanding is that Bicarb via the bohr effect is converted into CO2 and H20, removing H+ from the circulatory system.

When you are hypeprventilating a patient it is extremely difficult to get PCO2 below certain levels (15ish). Therefore a very acidotic patient breathing with an adequate tidal volume and 30 resp/minute has already diminished PCO2 maximally. The additional Bicarb will be hard to "blow off".

Additionally Bicarb can worsen lactic acidosis, as bicarb inhibits the unloading of O2 to tissues thus worsening hyperlactatemia (by inhibiting Ox-phos). therefore, Bicarb use in anion gap acidosis is generally not useful.

Bicarb is great for acidemic hyperK and TCA as mentioned.

One way to reduce acidosis peri-intubation is to have a ventilator in the room. Place the patient on SIMV prior to drugs and once sedating/paralying patient turn rate to 12, PS 10, PEEP 5, 100% FiO2 while you are waiting for sedative and paralytic to take effect (yes this is not RSI, but we dont want traditional RSI in a severely acidotic patient as risks of aspiration outweighed by acidosis-induced dysrhythmias). Get the tube in immediately, and crank up the RR trending capnography. Initial ETCO2 may be 10-15 (via NC if you have it), post-intubation if it goes up, you know you need to increase your rate.

Think this works better than bicarb, but not alot of evidence out there on this, just preference which I stole from anesthesia folks.

Originally Posted by ORL10

One way to reduce acidosis peri-intubation is to have a ventilator in the room. Place the patient on SIMV prior to drugs and once sedating/paralying patient turn rate to 12, PS 10, PEEP 5, 100% FiO2 while you are waiting for sedative and paralytic to take effect

Uh, SIMV prior to drugs? As in, awake intubation or are you using some sort of CPAP vent with a mask?

Originally Posted by Dr.McNinja

Uh, SIMV prior to drugs? As in, awake intubation or are you using some sort of CPAP vent with a mask?

So its not an awake intubation its really just preoxygenating the patient without having an RT bag. Bagging by RT's especially with an adult ambu-bag can overventilate patients significantly and result in greater gastric distension. In order to minimize this you can use a preset TV on a ventilator, and the insp flow time/rate given by a ventilator is produced by a machine > RT with sick patient.

SO prior to intubation patient has a CPAP/BiPap mask attatched to vent on SIMV mode (NOT A NON-INVASIVE MACHINE). Set to SIMV mode RR 0 TV 500, FiO2 100%, some people turn the flow rate down as well (reduce the insp time, but if you forget I dont think its a huge deal), Peep 5-8, PS 10-12 (like non-invasive for your COPDer's and CHF'ers).

Then when you are intubating and the etomidate/ketamine/propofol etc is going in you turn the rate to 12-14 and open the patients airway with a jaw thrust (usually the RT does this for you).
*this is where we differ from RSI, wait for sedation and paralytic to take effect patient still being ventilated because any hypoventilation will drop the pH and increase the pCO2 in a compensatory resp alkalosis patient very quickly.

Just after the tube goes in increase the RR as above.

Just an alternative to bicarb, and to bagging.

Originally Posted by Arch Guillotti

Disclaimer: The following may not be helpful to ED physicians.

I have found bicarb to be incredibly helpful when patients are very acidotic, hemorrhaging and circling the drain. With the administration of bicarb in a dire situation I have seen patients perk up immediately, CO2, BP, pulse ox and HR. Of course this is a temp fix that may allow pressors to work better as well.

In general I'm not a bicarb believer, but some of our cardiac ICU attendings swear by it too. I've seen NIRS and end tidal CO2 improve dramatically (albeit temporarily) in situations like you describe, though I admit there's no data to support doing it.

Originally Posted by Stitch

In general I'm not a bicarb believer, but some of our cardiac ICU attendings swear by it too. I've seen NIRS and end tidal CO2 improve dramatically (albeit temporarily) in situations like you describe, though I admit there's no data to support doing it.

Its completely anecdotal and probably doesn't make a difference in the long term but I swear by it too.

i think scott weingart had a great acidosis podcast (emcrit) on this topics a few months back...

Originally Posted by Stitch

In general I'm not a bicarb believer, but some of our cardiac ICU attendings swear by it too. I've seen NIRS and end tidal CO2 improve dramatically (albeit temporarily) in situations like you describe, though I admit there's no data to support doing it.

Originally Posted by Arch Guillotti

Its completely anecdotal and probably doesn't make a difference in the long term but I swear by it too.

It makes sense. You get a large immediate CO2 load from pushing a dose of bicarb. That increase in CO2 will dilate the cerebral vessels and allow for increased cerebral blood flow, which should shift the oxygen supply/demand equation toward excess supply. The NIRS would see that as increased residual oxygenation (it's biased 75% venous 25% arterial) and give a higher CrO2%. It's the practical effect of pH-stat management. During cardiopulmonary bypass if the NIRS is low the first thing we'll do is increase the MAP, then CO2. Transfusion if still low and hemoglobin marginal.

The CO2 load of bolus bicarb is also why it's a terrible idea to give it to someone who isn't mechanically ventilated or otherwise able to increase their own minute ventilation.