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The calculated value of the anion gap should always be adjusted for variations in the serum albumin concentration. [15] For example, in cases of hypoalbuminemia the calculated value of the anion gap should be increased by 2.3 to 2.5 mEq/L per each 1 g/dL decrease in serum albumin concentration (refer to Sample calculations, below).
An anion gap is usually considered to be high if it is over 12 mEq/L. High anion gap metabolic acidosis is typically caused by acid produced by the body. More rarely, it may be caused by ingesting methanol or overdosing on aspirin. [1] [2] The delta ratio is a formula that can be
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). Base deficit with normal anion gap indicates loss of bicarbonate (e.g., diarrhea).
The normal value for the anion gap is 8–16 mmol/L (12±4). An elevated anion gap (i.e. > 16 mmol/L) indicates the presence of excess 'unmeasured' anions, such as lactic acid in anaerobic metabolism resulting from tissue hypoxia, glycolic and formic acid produced by the metabolism of toxic alcohols, ketoacids produced when acetyl-CoA undergoes ...
Urine anion gap is calculated by subtracting the urine concentration of chloride from the concentrations of sodium plus potassium (): [3] = [+] + [+] [] where the concentrations are expressed in units of milliequivalents/liter (mEq/L).
Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap. [3]
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.
[8] During metabolic acidosis, a decrease in pH stimulates chemoreceptors. Peripheral chemoreceptors are found in the aortic and carotid bodies and respond to changes in the PaCO2, the arterial partial pressure of carbon dioxide. Central chemoreceptors are found in the brainstem and respond primarily to decreased pH in the cerebrospinal fluid ...