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Saturday, May 29, 2010

Lactic Acid

Lactic acid is produced and used in the body as a part of carbohydrate metabolism. Under normal circumstances this molecule is very useful to the body and plays an integral role in supplying the body with the energy it needs. However when metabolism is upset due to illness or injury lactic acid can build up in the tissues and the blood. Clinicians can monitor the levels of lactic acid in the body to monitor some disease states and their respective treatments.

Lactic acid is produced and used by the body. All cells can break glucose down into pyruvate via glycolysis; the first step of carbohydrate metabolism. This occurs in the cytoplasm of all cells. Pyruvate is broken down further to produced ATP. This is done in two ways. It can either diffuse into the mitochondria of a cell in order to enter into the Citric Acid cycle (Krebs cycle) or it can be broken down into lactate by lactate dehydrogenase. The Citric Acid cycle produces more ATP and less waste in comparison to the amount of ATP produced when lactate is made. However not all cells have mitochondria (i.e. erythrocytes) nor is there always enough oxygen present in cells to run the Citric Acid cycle. The main producers of lactate are skeletal muscle, erythrocytes, the brain, and the gut. The lactate produced by these cells will diffuse out into the blood stream and be picked up by another group of cells who will convert lactate back to glucose. Lactate metabolizers include the cells of the liver, the heart, and the kidneys.

When the body does not have an adequate supply of oxygen for glucose metabolism pyruvate is converted to lactate in the cells. The ATP created is then hydrolyzed to release the energy needed from its phosphate bond. The byproducts of this reaction are hydrogen ions, ADP, and a Pi ion. Under the normal conditions of the Citric Acid cycle these products would be recycled in the presence of oxygen, however in a hypoxic environment the constant hydrolysis of ATP leads to the accumulation of hydrogen ions causing a state of acidosis. It is important to note that it is the accumulation of these hydrogen ions and not the accumulation of lactate that causes acidosis. As lactate molecules leave a cell they give up a hydroxyl anion (OH-) and pick up a hydrogen ion to form lactic acid. The spare hydroxyl anion picks up another hydrogen ion to form water. This is one way that the excess hydrogen ions are buffered out. Lactate also acts as a buffer in that it can absorb extra hydrogen ions in the reverse reaction back into pyruvate via the enzyme lactate dehydrogenase. This occurs naturally as needed. In a healthy person these buffering capabilities are enough to keep the body balanced and avert a possible acidosis state; however under the conditions of illness and tissue hypoxia lactate production can spiral out of control and add to the problem.

Lactate levels are drawn by clinicians in order to evaluate and monitor conditions where there is a chance that tissue hypoxia or acidosis is occurring. Such conditions include sepsis, shock, heart attack, coma, seizures, uncontrolled diabetes, liver failure, and renal failure. Because lactate is normally being made in the body the normal range in plasma is around 0.4-2.0 mmol/L. A patient is generally considered to have hyperlactatemia once lactate levels rise between 4-5 mmol/L. Hyperlactatemia is a state of increased lactate levels with adequate tissue oxygenation and adequate acid-base balance. This can occur in liver failure and sepsis patients before tissue hypoperfusion sets in. The National Surviving Sepsis Campaign recommends that all patients at risk for sepsis have a baseline lactate level drawn upon admission and all patients with a lactate level >4 mmol/L are entered into special early goal-directed therapy. Hyperlactatemia is different from lactic acidosis. Lactic acidosis is the term given when lactate levels are increased and there is a disruption in the acid-base balance creating a state of acidosis. There are two levels of lactic acidosis. Type A is lactic acidosis with poor tissue perfusion and Type B is lactic acidosis with normal tissue perfusion. Type A cases are usually due to events that cut off oxygen supply such as shock, heart attacks, and strokes. Type B cases are usually due to illnesses such as diabetes, liver failure, drugs, toxins, and inborn errors of metabolism. Lactate can also be measured in cerebrospinal fluid. Lactate levels in CSF will be increased in the event of strokes, intracranial hemorrhage, epilepsy, and most importantly bacterial meningitis. Lactate levels in CSF are usually ordered in order to distinguish between bacterial and viral meningitis. Normal levels for lactate CSF are around 0.6-2.2 mmol/L.

Lactate levels are not a diagnostic marker of disease; rather they are another tool provided by the laboratory that clinicians can use to monitor disease states. When used in conjunction with other testing, lactate levels can tell a clinician whether or not a patient is metabolizing glucose correctly. It can also show that the body is metabolizing lactate correctly. A lactate level in conjunction with other testing can show whether or not the body is getting enough oxygen. More importantly this test can be used as a marker for monitoring patient treatment. It is currently the gold standard test to start and monitor treatment for sepsis patients. It is both an interesting metabolite and an insightful test.

· Gunnerson, K., Sat, S. (2009). Lactic Acidosis. Emedicine from WebMD. Retrieved on December 20, 2009 from http://emedicine.medscape.com/article/167027-overview
· Lactate. (2009). Lactate: The Test. Lab Tests Online. Retrieved on December 20, 2009 from http://www.labtestsonline.org/understanding/analytes/lactate/test.html
· Serum Lactate Measured. (2009). Implement the Sepsis Resuscitation Bundle: Serum Lactate Measured. Institute for Healthcare Improvement. Retrieved on December 20, 2009 from http://www.ihi.org/IHI/Topics/CriticalCare/Sepsis/Changes/IndividualChanges/SerumLactateMeasured.htm
· Kraviz, L. (2004). Lactate: Not Guilty as Charged. Retrieved on December 20, 2009 from http://www.unm.edu/~lkravitz/Article%20folder/lactate.html
· Burtis, C. A., Ashwood, E. R., Bruns, D. E., Tietz Textbook of Clinical Chemistry & Molecular Diagnostics. St. Louis, Missouri: Elsevier (2006). p. 877-878.

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