Capnography with Ketoacidosis

TheGodfather

TheGodfather

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I just thought I'd share something with you all that I discovered while working yesterday. My guess is the guru's out there know this, but it took me by surprise so I thought I'd share.

Before I begin, a little about me: Whenever I have patients with "legitimate" respiratory distress/compromise I'm ALWAYS using capnography (just for continued RR and continued waveform analysis -- not to mention the continued ETCO2 monitoring)...

ANYWAY; so late last night we get called to a resp distress. Long story short, it's DKA (kussmauls, "fruity odor", sugar "high", etc etc). This just so happens to be my first run-in with DKA in my 2-year career. Now, from what I understand from the pathophysiology of DKA is the following:

  • Metabolic Acidosis
  • Severe dehydration/electrolyte loss secondary to compensation of the acidosis
  • Inc respirations (Kussmauls) to compensate for acidosis and for the body to attempt to level out acid-base balance

From my prior understanding, I was told that the kussmauls were the body's way of blowing off excess CO2. So, after my initial treatment of fluids is going, I think, "what the heck, I'll slap on my capnography and see what's going on."

To my surprise, the ETCO2 on this patient was LOW (ranging from 9-13). Mind=Blown. From school I was always told "the patient is presenting with kussmauls to blow off excessive CO2. While yes, that may be the case, I forgot that the respiratory rate was in the high 30's consistently. CO2 is being blown out VERY fast, and the deep breaths are ensuring EXCESS O2 to the body.

Long story short, although the patient WAS indeed compensating by blowing off excess acidic gasses from the body, he was still HYPERVENTILATING causing the low ETCO2. So if any of you are like me out there and utilize your capnography regularly, do not be surprised if you see low ETCO2 with DKA. This is completely expected.
 
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Yup... the body is attempting to get rid of the excess acidosis, but it's not necessarily a very efficient method of doing so under these circumstances, which is why the EtCO2 will be low, but the blood acidosis will still be quite high.


Tis why when you get a hyperventilatory patient, you still need to do your due diligence before shrugging it off as a panic attack, even if they say they aren't diabetic.
 
And they also might not be drunk. That's ketones they're blowing off as well. If you get a chance to hang around and wait for RT to draw gases, you probably see a pH=<7.3, PaCO2=+/-5 torr from your EtCO2, PaO2=>100, HCO3=~9, BE=<-10, and SaO2=99% on RA. Remember their problem is not Respiratory. It's all metabolic.
 
MSDeltaFlt said:
And they also might not be drunk. That's ketones they're blowing off as well. If you get a chance to hang around and wait for RT to draw gases, you probably see a pH=<7.3, PaCO2=+/-5 torr from your EtCO2, PaO2=>100, HCO3=~9, BE=<-10, and SaO2=99% on RA. Remember their problem is not Respiratory. It's all metabolic.
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Very good point! Sheesh, I'm kicking myself after reading this for not knowing ABG's better -- welp, off to study!
 
Also consider that the ETCO2 may or may not match the PaCO2, and that to diagnose metabolic acidosis or respiratory alkalosis or whatever you'd need to know the pH and the bicarb--you'd an artertial blood gas, in other words. The ETCO2 gives you a clue, but you need more pieces of the puzzle to make a diagnosis.
 
Not a problem....like I said, any questions, let me know. I used to teach this crap. However, as I pointed out, that's not the book for you until you get the basics down because it gets really, really into the nitty gritty of blood gas physiology and can confuse anyone without a damn strong foundation in the basics.
 
Linuss said:
Yup... the body is attempting to get rid of the excess acidosis, but it's not necessarily a very efficient method of doing so under these circumstances, which is why the EtCO2 will be low, but the blood acidosis will still be quite high.
Click to expand...

However, were they breathing at a normal rate, their ETCO2 would likely be elevated.
 
jjesusfreak01 said:
However, were they breathing at a normal rate, their ETCO2 would likely be elevated.
Click to expand...

The acidosis isn't from CO2 its primarily from ketones released as a byproduct of the breakdown of fatty acids that aren't used by the cells for energy during a hyperglycemic episode. Remember its a metabolic acidosis not a respiratory acidosis.
 
NVRob said:
The acidosis isn't from CO2 its primarily from ketones released as a byproduct of the breakdown of fatty acids that aren't used by the cells for energy during a hyperglycemic episode. Remember its a metabolic acidosis not a respiratory acidosis.
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Right, but metabolic acidosis can still cause increased ETCO2 levels in our patients if they aren't blowing it off well? The difference with metabolic acidosis is the cause (not respiratory) and the fact that if its the body will be using the renal compensation mechanism. Of course, we can't do ABGs in the field, so its slightly more difficult for us to determine the cause of acidosis or alkylosis than it would be in a hospital.
 
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