Figure 618

Lactate-producing and lactate-consuming tissues under basal conditions and pathogenesis of lactic acidosis. Although all tissues pro-

Causes of metabolic acidosis tabulated according to the prevailing pattern of plasma electrolyte composition. Assessment of the plasma unmeasured anion concentration (anion gap) is a very useful first step in approaching the differential diagnosis of unexplained metabolic acidosis. The plasma anion gap is calculated as the difference between the sodium concentration and the sum of chloride and bicarbonate concentrations. Under normal circumstances, the plasma anion gap is primarily composed of the net negative charges of plasma proteins, predominantly albumin, with a smaller contribution from many other organic and inorganic anions. The normal value of the plasma anion gap is 12 ± 4 (mean ± 2 SD) mEq/L, where SD is the standard deviation. However, recent introduction of ion-specific electrodes has shifted the normal anion gap to the range of about 6 ± 3 mEq/L. In one pattern of metabolic aci-dosis, the decrease in bicarbonate concentration is offset by an increase in the concentration of chloride, with the plasma anion gap remaining normal. In the other pattern, the decrease in bicarbonate is balanced by an increase in the concentration of unmeasured anions (ie, anions not measured routinely), with the plasma chloride concentration remaining normal.

duce lactate during the course of glycolysis, those listed contribute substantial quantities of lactate to the extracellular fluid under normal aerobic conditions. In turn, lactate is extracted by the liver and to a lesser degree by the renal cortex and primarily is reconverted to glucose by way of gluconeogenesis (a smaller portion of lactate is oxidized to carbon dioxide and water). This cyclical relationship between glucose and lactate is known as the Cori cycle. The basal turnover rate of lactate in humans is enormous, on the order of 15 to 25 mEq/kg/d. Precise equivalence between lactate production and its use ensures the stability of plasma lactate concentration, normally ranging from 1 to 2 mEq/L. Hydrogen ions (H+) released during lac-tate generation are quantitatively consumed during the use of lactate such that acid-base balance remains undisturbed. Accumulation of lactate in the circulation, and consequent lactic acidosis, is generated whenever the rate of production of lactate is higher than the rate of utilization. The pathogenesis of this imbalance reflects overproduction of lactate, underutilization, or both. Most cases of persistent lactic acidosis actually involve both overproduction and underutiliza-tion of lactate. During hypoxia, almost all tissues can release lactate into the circulation; indeed, even the liver can be converted from the premier consumer of lactate to a net producer [1,14].

Muscle Brain Skin n n

Anaerobic glycolysis

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