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#1 |
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Semper Ubi Sub Ubi
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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
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EM/Med Tox Attending +-+ one should never underestimate the predictability of stupidity. don't panic. |
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#2 |
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Nobel War Prize Winner
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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. |
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#3 |
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Member
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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? Last edited by Groove; 09-19-2011 at 11:03 AM. |
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#4 |
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Senior Member
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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
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What is the most stable rhythm? NO!! It is not NSR! Asystole is the ultimate form of stabilization! |
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#5 |
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Senior Member
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TCA overdoses with QRS widening
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#6 |
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Senior Member
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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, . . .
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