|Bicarbonate & Anion Gap|
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Bicarbonate on the chemistry panel gives you an indication of acid-base status, but does not replace blood gas measurement as it does not supply information about the respiratory component of acid-base maintenance. Bicarbonate values should always be interpreted with the anion gap, which is a calculated parameter. The anion gap provides useful information for delineating causes of metabolic acidosis and can give you an indication of a mixed acid-base disturbance.
In health, blood pH (which is taken as the same as ECF pH) is maintained within a narrow range of approximately 7.4 to 7.5. Traditional interpretation of acid-base status involves the Henderson-Hasselbach equation, where pH is determined by the ratio of bicarbonate to carbon dioxide. Blood pH is normal when the ratio of HCO3- to pCO2 is 20:1. Respiratory factors affect pCO2, whereas non-respiratory, or metabolic factors, affect the HCO3-.
The major extracellular buffer of acids in the body is bicarbonate followed by plasma proteins and bone. Intracellular buffers include proteins, organic phosphate, inorganic phosphate and hemoglobin (in erythrocytes). Regulation of acid-base involves chemical buffering with intra- and extra-cellular buffers, control of partial pressure of carbon dioxide by altering respiration and control of bicarbonate and hydrogen excretion by the kidneys. In general, rapid changes in acid-base can be achieved by changing respiration, whereas the kidney is involved in slower, more long-term regulation of acid-base status. The kidney is central to acid-base regulation. Filtered bicarbonate is absorbed in the PCT of the kidney and regenerates the bicarbonate lost in buffering acids produced by normal body metabolism. Hydrogen is excreted by the PCT and DCT of the kidney. Excretion of H+ by the PCT is dependent on filtered phosphates and urea generated by the tubular epithelial cells. Excretion of H+ by the DCT is dependent on sodium resorption and exchanges for K+.
The non-traditional approach to acid-base status involves independent and dependent variables. Independent variables are pCO2, strong ion difference (difference between Na and Cl) and nonvolatile weak acids (plasma proteins). These alter dependent variables which are bicarbonate and H+. This differs from traditional approaches to acid-base interpretation as it contends that any changes in bicarbonate are secondary to changes in plasma proteins, respiration and electrolytes. In theory, it is a more physiologic approach to acid-base abnormalities, however, in practice, using non-traditional approaches does not alter interpretations gleaned from traditional approaches.
There are four primary types of acid-base disorders: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. The majority of patients with acid-base imbalance have either metabolic acidosis or metabolic alkalosis or a mixed disorder of both.
Acidosis can be primary metabolic (decreased HC03) or respiratory (hypercapnea) or secondary in compensation for a primary alkalosis. Acidosis has profound effects on the body, resulting in arrythmias, decreased cardiac output, depression, and bone demineralization.
Alkalosis can be primary metabolic (increased HCO3) or respiratory (hypocapnea) or secondary in compensation for a primary acidosis. Usually respiratory alkalosis is the compensatory mechanism for a primary metabolic acidosis. Alkalosis results in tetany and convuulsions, weakness, polydipsia and polyuria.
In general, changes in bicarbonate produce compensatory changes in carbon dioxide and vice versa. Compensation causes parallel changes in pCO2 and bicarbonate.
In a primary metabolic acidosis, HCO3 will be decreased. The compensatory response is reduction of pCO2 by alveolar hyperventilation (i.e. a secondary respiratory alkalosis), e.g. dogs with a lactate acidosis from hypovolemia often hyperventilate. The maximum respiratory compensation expected for a primary metabolic acidosis is estimated from the following formula:
Decrease in pCO2 = 1.5 [HCO3) + 8
The compensatory response for a primary respiratory acidosis is renal retention of bicarbonate (a secondary metabolic alkalosis).
In a primary metabolic alkalosis, HCO3 is increased. Chemoreceptors in the respiratory center sense the alkalosis and trigger hypoventilation, resulting in increased pC02 or a compensatory respiratory acidosis.
The compensatory response to a respiratory alkalosis is initially due to a decrease in ECF bicarbonate from cellular buffering. Then renal resorption of bicarbonate is reduced. The decline in bicarbonate is offset by retention of chloride (to maintain electroneutrality), thus producing a secondary hyperchloremic metabolic acidosis. The pH can revert to normal from compensation in chronic respiratory alkalosis.
Remember these rules for compensation:
Characteristic findings in the different primary acid-based disorders with appropriate compensatory changes are illustrated in the table below.
Mixed acid-base disturbances