Here's how it works:
In the cytosol, pyruvate turns into lactate (rather than move towards acetyl-CoA) for a number of reasons, again that I'm not going to get into, via lactate dehydrogenase. That lactate (via shuttles) gets to the cytosol of the liver and kidneys where it eventually makes its way into the Cori/Lactic Acid Cycle. The Cori cycle eventually spits out glucose. So far so good, right? Glucose via glycolysis seems to be metabolized into lactate, ATP, and water. Said ATP gets hydrolyzed into ADP and inorganic phosphate which releases that very necessary proton (H+). When conditions get revved up, i.e. septic shock, and an excess of lactate is being produced, then the cell cannot handle the metabolism of lactate and guess what's also being overproduced? Said H+ which tags onto the lactate creating lactic acid.
The articles I've read tend to say that you start running into lactic acidosis territory when you have a lactate 5 with a concurrent acidosis (pH less than 7.35).
Mad props to Amanda, my pharmacist teammate, for listening to me and helping me work through this while not making too much fun of me.
<7 .35="" additional="" again.="" and="" any="" are....="" be="" better.="" biochemistry="" br="" can="" definitely="" did="" diving="" going="" help="" here="" i="" into="" knowledge="" me="" nbsp="" never="" of="" or="" others="" pointers="" provide="" think="" this="" to="" understand="" was="" we="" welcome="" you="">
Link to article (NOT FREE)
Fall P, Szerlip H. Lactic acidosis: from sour milk to septic shock. J Intensive Care Med 2005; 20: 255-71.
Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
In the cytosol, pyruvate turns into lactate (rather than move towards acetyl-CoA) for a number of reasons, again that I'm not going to get into, via lactate dehydrogenase. That lactate (via shuttles) gets to the cytosol of the liver and kidneys where it eventually makes its way into the Cori/Lactic Acid Cycle. The Cori cycle eventually spits out glucose. So far so good, right? Glucose via glycolysis seems to be metabolized into lactate, ATP, and water. Said ATP gets hydrolyzed into ADP and inorganic phosphate which releases that very necessary proton (H+). When conditions get revved up, i.e. septic shock, and an excess of lactate is being produced, then the cell cannot handle the metabolism of lactate and guess what's also being overproduced? Said H+ which tags onto the lactate creating lactic acid.
The articles I've read tend to say that you start running into lactic acidosis territory when you have a lactate 5 with a concurrent acidosis (pH less than 7.35).
Mad props to Amanda, my pharmacist teammate, for listening to me and helping me work through this while not making too much fun of me.
<7 .35="" additional="" again.="" and="" any="" are....="" be="" better.="" biochemistry="" br="" can="" definitely="" did="" diving="" going="" help="" here="" i="" into="" knowledge="" me="" nbsp="" never="" of="" or="" others="" pointers="" provide="" think="" this="" to="" understand="" was="" we="" welcome="" you="">
Link to article (NOT FREE)
Fall P, Szerlip H. Lactic acidosis: from sour milk to septic shock. J Intensive Care Med 2005; 20: 255-71.
Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
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