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Anion gap can be classified as either high, normal or, in rare cases, low. Laboratory errors need to be ruled out whenever anion gap calculations lead to results that do not fit the clinical picture. Methods used to determine the concentrations of some of the ions used to calculate the anion gap may be susceptible to very specific errors.
The anion gap (AG) without potassium is calculated first and if a metabolic acidosis is present, results in either a high anion gap metabolic acidosis (HAGMA) or a normal anion gap acidosis (NAGMA). A low anion gap is usually an oddity of measurement, rather than a clinical concern.
Diarrhea, in which large amounts of bicarbonate are excreted; Ingestion of poisons such as methanol, ethylene glycol, or excessive aspirin; The serum anion gap is useful for determining whether a base deficit is caused by addition of acid or loss of bicarbonate. Base deficit with elevated anion gap indicates addition of acid (e.g., ketoacidosis).
Urine NH 4 + is difficult to measure directly, but its excretion is usually accompanied by the anion chloride. A negative urine anion gap can be used as evidence of increased NH 4 + excretion. In a metabolic acidosis without a serum anion gap: A positive urine anion gap suggests a low urinary NH 4 + (e.g. renal tubular acidosis).
The anion gap is calculated by subtracting the sum of the serum concentrations of major anions, chloride and bicarbonate, from the serum concentration of the major cation, sodium. (The serum potassium concentration may be added to the calculation, but this merely changes the normal reference range for what is considered a normal anion gap)
Most of the carbonic acid then dissociates to bicarbonate and hydrogen ions. The bicarbonate buffer system is an acid-base homeostatic mechanism involving the balance of carbonic acid (H 2 CO 3), bicarbonate ion (HCO − 3), and carbon dioxide (CO 2) in order to maintain pH in the blood and duodenum, among other tissues, to support proper ...
Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and an increase in plasma chloride concentration [1] (see anion gap for a fuller explanation).
Diagnosis of contraction alkalosis is made by correlating laboratory data with clinical history and examination. Metabolic alkalosis in the presence of decreased effective circulatory volume, loop diuretic use, or other causes of intravascular depletion such as profound diarrhea should raise suspicion for contraction alkalosis as a likely etiology in the absence of other causes.