Lactic Acidosis

This is a follow up to the conversation about lactate metabolism during rounds a few days ago:

As you all remember, during times of low oxygen delivery (i.e. decreased perfusion) or mitochrondiral dysfunction (for example, cyanide poisoning), the pyruvate produced during glycolysis by skeletal muscle is shunted away from the Krebs cycle (aerobic metabolism) and instead converted by LDH into lactate (anaerobic metabolism).  When intracellular lactate (an anion) is released into the blood a cation (H+) must follow, thus producing an acidosis.  

Lactate is not only produced during times of low oxygenation but also during routine functions.  This lactate is taken up by mitochrondia in hepatocytes and converted back to glucose via gluconeogenesis.  This is known as the Cori Cycle (Gerty & Cari Cori won the Nobel Prize in 1947) or Lactic Acid Cycle.

Lactic acidosis develops whenever there rapid increase in lactate production (type A lactic acidosis) overwhelming the ability of the hepatocytes to clear it, about 5mM/L.  Also, lactate can build up due to dysfunction within the hepatocytes decreasing the ability to clear lactate (type B lactic acidosis).

On the trauma service, type A lactic acidosis due to hypoperfused tissues is the more common presentation of the disorder.

Treatment is restoration of normal blood flow by stopping bleeding and replacing blood volume.  Buffering agents (Na Bicarb, THAM, Carbicarb) can be considered for pH less than 7.2 but these have limited value because the underlying problem is not being corrected and the agents themselves can have negative consequences.  

Thanks to Dr. Mike Dingeldein for putting this together.