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Lactic Acid. Lactic acid is fuel for your cells during intense exercise. It’s created when your body breaks down glucose and other carbohydrates. It’s a common myth that muscle soreness you feel after exercise is caused by lactic acid trapped in your cells. Studies have found that’s not true. Federal government websites often end in. Before sharing sensitive information, make sure you're on a federal government site.
The site is secure. NCBI Bookshelf. Chris D. Foucher ; Robert E. Authors Chris D. Foucher 1 ; Robert E. Tubben 2. Lactic acid is produced in physiologically normal processes, and as a common finding in disease states. When increased production is comorbid with decreased clearance, the severity of the clinical course escalates. Importantly, the effects of severely elevated levels of lactic acid can have profound hemodynamic consequences and can lead to death.
Serum lactate levels can be both a marker for risk as well as a therapeutic target. The higher the level and the longer the time to normalization of elevated serum lactate, the greater the risk of death. This activity reviews the etiology, presentation, evaluation, and management of lactic acidosis, and reviews the role of the interprofessional team in evaluating, diagnosing, and managing the condition.
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Objectives: Review the etiologies of lactic acidosis. Outline the presentation of lactic acidosis and the examination findings that can confirm its diagnosis, including necessary lab work. Summarize the available treatment and management strategies for lactic acidosis. Explain the importance of improving coordination amongst the interprofessional team to enhance care for patients affected by lactic acidosis.
Access free multiple choice questions on this topic. Clinicians should be aware that hyperlactatemia can occur in the presence of adequate tissue perfusion and oxygenation. Lactic acidosis on the other hand usually occurs in the presence of inadequate tissue perfusion, abnormalities in carbohydrate metabolism and with the use of certain medications. It is then metabolized mostly via the liver and the kidney.
Some tissues can use lactate as a substrate and oxidize it to carbon dioxide C02 and water, but only the liver and kidney have the necessary enzymes to utilize lactate for the process of gluconeogenesis. The tissues which normally produce excess lactic acid include the skin, red cells, brain tissue, muscle, and the gastrointestinal GI tract. During heavy exercise, it is the skeletal muscles which produce the most excess circulating lactate, which normalizes in the absence of impaired hepatic metabolism.
In general, elevated lactate can be the result of increased production, decreased clearance, or both.
Pyruvate production as a result of glycolysis gets shunted into two main metabolic pathways. Under aerobic conditions, it enters the citric acid cycle after having been converted to acetyl-CoA by pyruvate dehydrogenase, and a series of reactions occur to form ATP and NADH, which goes on to the process of oxidative phosphorylation which produces the majority of ATP in a cell. However, under anaerobic conditions, pyruvate generated from glycolysis channels into the Cori cycle or lactic acid cycle.
Excess lactate gets shuttled to the liver, to undergo gluconeogenesis. Pathologic and persistent lactic acidosis occurs when a combination of two variables coexist.
Lactic Acidosis: What You Need to Know
For example, excessive lactate production from severe convulsions concomitant with impaired hepatic metabolic capabilities such as can occur with cirrhosis, hypothermia, sepsis, severe hypovolemia, severe hypotension, or some combination of these factors, can lead to severe lactic acidosis. Lactic acidosis is among the most common concerns for those caring for critically ill patients. However, clinical studies of this problem have been somewhat sparse, with most studies being retrospective, or prospective with small sample sizes.
Jung et al. The severity of lactatemia and the time for the lactic acidosis to correct were linked to survival. The higher the level and the longer the time for normalization, the greater the mortality. Shock and severe lactic acidosis pH less than 7. No survival has been reported for severe lactic acidosis with shock when the pH had fallen under 7. Interestingly, this contrasts to lactic acidosis associated with non-shock states, as in metformin-induced lactic acidosis producing pH values of 7.
Other definitions for lactic acidosis include pH less than or equal to 7. High levels of lactate are associated with increased risk of death independent of organ failure and shock. Patients with mildly elevated and intermediate levels along with sepsis have higher rates of in-hospital day mortality.