Influence of steady-state alterations in acid-base equilibrium on the fate of administered bicarbonate in the dog.

Abstract

A B S T R A C T Previous workers have shown that metabolic acidosis increases the apparent space through which administered bicarbonate is distributed. This finding has been ascribed to the accompanying acidemia and to the consequent availability of a large quantity of hydrogen ion that accumulates on nonbicarbonate tissue buffers during the development of acidosis. To test this hypothesis, bicarbonate space was measured in dogs with a broad range of steady-state plasma [HCO-] in association with alkalemia as well as with acidemia. Appropriate combinations of pH and plasma [HCO-] were achieved by pretreating the animals to produce graded degrees of each of the four cardinal, chronic acid-base disorders. Metabolic acidosis (n = 15) was produced by prolonged HCI-feeding; metabolic alkalosis (n = 17) by diuretics and a chloride-free diet; and respiratory acidosis (n = 9) and alkalosis (n = 8) by means of an environmental chamber. Animals with normal acid-base status (n = 4) were also studied. Sodium bicarbonate (5 mmol/kg) was infused over 10 min to the unanesthetized animals; observations were carried out over 90 min.

Dietary Acid, Age, and Serum Bicarbonate Levels among Adults in the United States

“…Therefore, high dietary acid could produce the sequelae of a subclinical acidosis in these younger adults even without observable differences in plasma acid-base parameters. Intracellular buffering would blunt the effect of NEAP on extracellular buffers, and buffering capacity likely varies directly with the serum bicarbonate (33). Thus, the change in bicarbonate might particularly underestimate the effects of NEAP among older persons, who had the highest bicarbonate levels in our sample.…”

Intradialytic Hypercapnic Respiratory Failure Managed by Noninvasive Assisted Ventilation

“…The intradialytic decrease or minimal increase in blood bicarbonate levels associated with increases in PCO 2 level, indicate an excessive bicarbonate buffering and CO 2 production. This augmented buffering was probably due to multiple factors including severe metabolic acidosis, malnutrition and intradialytic tissue hypoxia, induced by congestive heart failure, peripheral vascular disease and intradialytic hypotension [1][2][3][4][5][6]. The higher dialysate bicarbonate concentration needed to correct metabolic acidosis and counterbalance respiratory acidosis, was associated with increased CO 2 production, which in the presence of ventilatory failure resulted in exacerbation of the hypercapnia and the respiratory acidosis.…”

“…The dialysis procedure is associated with diffusion of bicarbonate from the dialysate to the blood, and its buffering by H + released from nonbicarbonate buffers in the intra-and extracellular compartments [1,2]. The extent of bicarbonate titration is related to the degree of predialysis metabolic acidosis and the intradialytic production of organic acids [3,4], which is augmented in the presence of tissue hypoxia or malnutrition [5,6].…”

The effect of hemodialysis on protein metabolism. A leucine kinetic study.

“…Bicarbonate gain = (post-HCO3 -pre-HCO ) X (BWX 0.4), where HCO3 represents serum bicarbonate levels post-and predialysis, BWis post dialysis body weight, and 0.4 represents bicarbonate distribution space or 40% of body weight. This 40% distribution appears to be appropriate for the pH ranges of our patients, 7.33-7.45 (26). Bicarbonate loss = [(pre-HCO-+ post-HCO )/2] x UF, where UF is ultrafiltration or fluid removal during dialysis.…”