Would Low blood sugar cause hypocapnia?

[tchristifulli]

You need glucose to initiate the Kreb cycle.. Right? So wouldn't your CO2 be lower as well? I assume that if your unresponsive in a diabetic coma your C02 might be elevated if your respiration are slow, but with a normal respiratory rate your ETC02 should be lower . Educate me people!

 

[chaz90]

Things aren't that quick to change. Remember, cells are still mostly acting normally in the body during a hypoglycemic unconscious episode. The person likely overdosed on insulin (or didn't eat), so their blood glucose level is low, but think about where that glucose went. Insulin is a hormone that activates glucose transporters into the cells from the blood, so intracellular glucose is normal/high and the cells are ticking along through cellular respiration just fine. We just don't measure intracellular glucose levels.

The unconsciousness is just because the brain requires a continuous supply of glucose directly and is very sensitive to rapid changes in BGL. That's also why it's so quick to fix though after a bit of D50.

 

[tchristifulli]

Makes Sence! Thanks man. So how long do you think it would be before you notice a change?

 

[chaz90]

I would imagine they'd die from prolonged hypoglycemia before it became an issue. As mentioned, I think the bigger problem would be hypercapnia and respiratory acidosis if ventilation became impaired.

 

[usalsfyre]

Now tchristifulli, I challenge you to explain why you're hypocapneic during a prolonged HYPERglycemic episode.

 

[DesertMedic66]

Now tchristifulli, I challenge you to explain why you're hypocapneic during a prolonged HYPERglycemic episode.

I'm gonna make a guess (that's probably wrong) and say possibly due to Kussmaul breathing?

 

[Anonymous]

I'm gonna make a guess (that's probably wrong) and say possibly due to Kussmaul breathing?

I'm gonna make a guess and say you are probably right.

 

[chaz90]

I'm gonna make a guess (that's probably wrong) and say possibly due to Kussmaul breathing?

What do the Kussmaul respirations come from though? They're a compensatory mechanism due to the acidosis inherent to DKA (which isn't necessarily happening in every episode of prolonged hyperglycemia). Increasing acidity leads to increasing CO2 levels, which has to be blown off by hyperventilation. These patients are technically physiologically hypercarbic and just appear hypocarbic on EtCO2 due to the increased respiratory rate blowing off the large quantities of CO2 in many smaller exhalations.

If I'm reading it right here, usalsfyre is asking what causes hypocarbia in patients that are hyperglycemic but not acidotic (could be totally wrong and reading way too much into this).

 

[teedubbyaw]

Now tchristifulli, I challenge you to explain why you're hypocapneic during a prolonged HYPERglycemic episode.

Metabolic acidosis compensated by Kussmaul breathing.