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Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids. [3]
Additionally, a loss of pyruvate carboxylase allows potentially toxic compounds, such as lactic acid and ammonia, to build up and damage organs and tissues. Loss of pyruvate carboxylase function in the nervous system, particularly the role of the enzyme in myelin formation and neurotransmitter production, may contribute to the neurological ...
Sepsis has a worldwide incidence of more than 20 million cases a year, with mortality due to septic shock reaching up to 50 percent even in industrialized countries. [ 35 ] According to the U.S. Centers for Disease Control , septic shock is the thirteenth leading cause of death in the United States and the most frequent cause of death in ...
Due to the lack of oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor in the electron transport chain, is not abundant, this slows down entry of pyruvate into the Krebs cycle, resulting in its accumulation. The accumulating pyruvate is converted to lactate (lactic acid) by lactate dehydrogenase.
The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is lactic acid, which disappears as blood flow and oxygen debt are corrected.
Lactic acidosis can result from increased anaerobic metabolism. However, the effect of acid–base balance can be variable as patients with large GI losses can become alkalotic. In cases of hemorrhagic shock, hematocrit and hemoglobin can be severely decreased. However, with a reduction in plasma volume, hematocrit and hemoglobin can be ...
Lactic acidosis arises from impairment of gluconeogenesis. Lactic acid is generated both in the liver and muscle and is oxidized by NAD + to pyruvic acid and then converted via the gluconeogenic pathway to G6P. Accumulation of G6P inhibits the conversion of lactate to pyruvate. The lactic acid level rises during fasting as glucose falls.
Other causes [citation needed] Ingestion of ammonium chloride, hydrochloric acid, or other acidifying salts; The treatment and recovery phases of diabetic ketoacidosis; Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3–4L can cause acidosis; Hyperalimentation (i.e., total parenteral nutrition)