Lactic Acidosis

We use lactate a lot, and it is mentioned specifically in the syllabus - it says we should be able to "understand the significance of lactic acidosis in the critically ill patient".

Pathophysiology
Lactate is produced by glycolysis and metabolised by the liver. It is commonly thought it is produced as a result of anaerobic metabolism, but this has been disproved. It is now thought that the adrenergic state and cytokine storm probably change glucose metabolism, changing lactate production.
Adrenaline stimulates beta-2 receptors which up-regulates glycolysis, generating more pyruvate than can be used by the cell’s mitochondria. This excess pyruvate is converted into lactate.  

Lactate can be used by the heart and brain as a fuel source, further suggesting lactate is a stress response.

Lactate clearance is reduced in hepatic failure. The utility of lactate clearance as a marker of disease severity is debated. Some suggest if the lactate level doesn't drop, lactate must still be being produced - so things are serious. The half life of lactate is about twenty minutes.

Measuring Lactate 
The lactate level is independent of anion gap and bicarb so does need to be checked. The level can be high, even if the blood pressure is low.
A venous level is fine, unless there's been a really prolonged tourniquet time when taking the sample!
If you're sending your tests to the lab, even at room temperature (not on ice) the value doesn't change).

Causes of High (>4) lactate
Sepsis
Exercise
Beta-agonist use (like salbutamol)
Even not on ice, the lactate value is unchanged for 15minutes at room temperature.

Treating a High Lactate 
Identify and treat the cause - it's not always sepsis
Remember, a high lactate is a marker of disease severity, not a marker of disease.
Hartmann's (ringers lactate) does not contain the right type of lactate, and does not affect the lactate level.
Remember nebulisers can cause a high latate - which might worsen the dyspnoea.

Causes of a High Lactate
Type A lactic acidosis is seen in states of hypoperfusion or poor oxygenation - shock and cardiac arrest
Type B lactic acidosis is seen in states of high metabolism, organ dysfunction, and toxins. This might be contributed to by thiamine deficiency, neoplastic cells, mitochondrial dysfunction (antiretroviral therapy, linezolid, propofol), hepatic dysfunction.

I haven't written a summary on this one - I think St Emlyns have summarised quite well!!

References
http://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/ 
http://www.emdocs.net/utility-obtaining-lactate-measurement-ed/
http://emj.bmj.com/content/32/9/670.full?hwoasp=authn%3A1451324344%3A4223703%3A1415336879%3A0%3A0%3AVUcQvREASLSBBNQdFnX7Aw%3D%3D
http://emcrit.org/wee/lactate-clearance-flawed/
http://www.heftemcast.co.uk/lactate-lactate-clearance/ 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427204/ 
http://emnerd.com/tag/lactate-clearance/ 
http://emcrit.org/wp-content/uploads/lactate-faq.pdf 
http://www.rcemfoamed.co.uk/portfolio/sepsis-in-the-ed/
http://www.aliem.com/blast-from-the-past-occult-sepsis-lactic-acid-and-mortality/
http://www.oapublishinglondon.com/article/431#
http://emcrit.org/wee/lactate-clearance-flawed/ 
http://www.ncbi.nlm.nih.gov/pubmed/9366769