Lactic acidosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* [[Lactic Acidosis|Lactic acidosis]] occurs when cells make lactic acid faster than it can be metabolized. <ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016</ref> <ref>Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X</ref> | *[[Lactic Acidosis|Lactic acidosis]] occurs when cells make lactic acid faster than it can be metabolized. <ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016</ref> <ref>Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X</ref> Both overproduction of lactate, or reduced metabolism, lead to acidosis. Normal lactate levels are less than two mmol/L, lactate levels between 2 mmol/L and 4 mmol/L are defined as hyperlactatemia. Severe hyperlactatemia is a level of 4 mmol/L or higher. Other definitions for lactic acidosis include pH less than or equal to 7.35 and lactatemia greater than 2 mmol/L with a partial pressure of carbon dioxide (PaC02) less than or equal to 42 mmHg. | ||
Acid generation on the cellular level is dictated by the ratio of oxidized (NAD+) and reduced (NADH) nicotinamide adenine dinucleotide. These molecules help maintain the intracellular pH by influencing the ratio of pyruvate to lactate. An increased NADH concentration results in an increased lactate level. Causes of increased NADH include a hypoxic state, ingestion and oxidation of large amounts of ethanol, etc. | |||
Lactic acidosis is an underlying process in the development of [[rigor mortis]]. Tissue in the muscles of the deceased resort to anaerobic metabolism in the absence of oxygen and significant amounts of lactic acid are released into the muscle tissue. This along with the loss of [[adenosine triphosphate|ATP]] causes the muscles to grow stiff. | Lactic acidosis is an underlying process in the development of [[rigor mortis]]. Tissue in the muscles of the deceased resort to anaerobic metabolism in the absence of oxygen and significant amounts of lactic acid are released into the muscle tissue. This along with the loss of [[adenosine triphosphate|ATP]] causes the muscles to grow stiff. | ||
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Pathophysiology
- Lactic acidosis occurs when cells make lactic acid faster than it can be metabolized. [1] [2] Both overproduction of lactate, or reduced metabolism, lead to acidosis. Normal lactate levels are less than two mmol/L, lactate levels between 2 mmol/L and 4 mmol/L are defined as hyperlactatemia. Severe hyperlactatemia is a level of 4 mmol/L or higher. Other definitions for lactic acidosis include pH less than or equal to 7.35 and lactatemia greater than 2 mmol/L with a partial pressure of carbon dioxide (PaC02) less than or equal to 42 mmHg.
Acid generation on the cellular level is dictated by the ratio of oxidized (NAD+) and reduced (NADH) nicotinamide adenine dinucleotide. These molecules help maintain the intracellular pH by influencing the ratio of pyruvate to lactate. An increased NADH concentration results in an increased lactate level. Causes of increased NADH include a hypoxic state, ingestion and oxidation of large amounts of ethanol, etc.
Lactic acidosis is an underlying process in the development of rigor mortis. Tissue in the muscles of the deceased resort to anaerobic metabolism in the absence of oxygen and significant amounts of lactic acid are released into the muscle tissue. This along with the loss of ATP causes the muscles to grow stiff.