Lactate
is a byproduct of glycolosis, which is an anaerobic glucose metabolism
occurring in the cellular cytoplasm.
Pyruvate is also generated through glycolosis and is broken down through
the Krebs cycle to create energy (Sharma 2007).
The liver’s lactate to glucose conversion ability decreases when there
are elevated blood levels of lactose (Sharma 2007). Once the liver can no longer maintain the
lactate to glucose conversion, acidosis begins. With adequate oxygen, adenosine
triphosphate (ATP) metabolites are recycled and cytosolic lactate concentration
increases without acidosis (Sharma 2007).
Hypoxia prompts cells to utilize anaerobic energy to create ATP
resulting in lactate and hydrogen (Sharma 2007). Sepsis accounts for most cases of lactic
acidosis (Sharma 2007).
Arterial blood gasses need to be
drawn in order to identify the current condition of our patient as well as a
full assessment. Continued monitoring
would be warranted during critical states of illness. Signs of impaired tissue perfusion consist of
hypotension, peripheral vasoconstriction, and oliguria (Sharma 2007). Signs of septic shock include tachypnia,
hypotension, and decreased mental status (Sharma 2007). The appropriate
treatment for this patient is to treat the underlying cause of the acidosis, in
other words, treat the pneumonia. In the
case of lactic acidosis, sodium bicarbonate may be given to balance the
pH. ABG and patient monitoring are
necessary to ensure appropriate treatment is being administered.

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