PCO2 and [K+]p in Metabolic Acidosis

Abstract

Studies by Schwartz and colleagues at Tufts University School of Medicine in the 1960s described the "whole-body" acidbase response (i.e., secondary changes in plasma [HCO 3 Ϫ ] to graded degrees of acute respiratory acidosis and acute respiratory alkalosis in humans (1,2). Corresponding data for acute metabolic acid-base disorders (i.e., secondary changes in PaCO 2 ) are essentially unavailable: meager observations have been made in acute metabolic alkalosis, and no data exist for acute metabolic acidosis. The report by Wiederseiner et al. (3) in this issue of JASN addresses the secondary physiologic response to acute mineral acid-induced metabolic acidosis in humans.In a carefully conducted study, the slope of the PCO 2 (arterialized)/[HCO 3 Ϫ ] relationship averaged 0.85 mmHg per mmol/L in six healthy male volunteers with acute NH 4 Clinduced metabolic acidosis who had attained an operational steady state (by convention, "acute" corresponds to the interval before any meaningful contribution of changes in renal acidification to plasma [HCO 3 Ϫ ]). The range of hypobicarbonatemia achieved in this study was limited (nadir of approximately 19 mmol/L); thus these data serve to define the limits of the ventilatory response to mild, acute metabolic acidosis in humans and enable consideration of the possible coexistence of respiratory acid-base disorders. Whether the same slope applies to more severe degrees of acute metabolic acidosis remains unknown.The observed slope is substantially less steep than that described for chronic metabolic acidosis in humans, which is on the order of 1.1 to 1.4 mmHg per mmol/L. However, the PaCO 2 /[HCO 3 Ϫ ] relationship in clinical chronic metabolic acidosis has by necessity been derived by simply correlating the available pathologic values of the two determinants of plasma acidity without regard for their deviation from the control baseline. When we compared the ventilatory response to chronic HCl-induced metabolic acidosis in a large cohort of dogs as obtained by computing the changes in PaCO 2 and plasma [HCO 3 Ϫ ] (i.e., experimental minus control valueswhat we consider as the appropriate methodology) versus only the experimental values, the significantly disparate slopes of 0.86 versus 1.20 mmHg per mmol/L, respectively, were obtained (4). In our opinion, the precise slope of the ventilatory response to chronic metabolic acidosis in humans remains uncertain.Furthermore, we have previously shown in dogs that acutely the secondary hypocapnia that accompanies metabolic acidosis leaves plasma [HCO 3 Ϫ ] undisturbed, thereby providing maximal defense of systemic pH (5). In stark contrast, in the chronic setting, secondary hypocapnia evokes a maladaptive renal response that yields a sizable reduction in plasma [HCO 3 Ϫ ] (beyond that attributed to the acid load itself) and diminishes the degree to which plasma acidity is potentially protected by the ventilatory response. Whether these observations are applicable to metabolic acidosis in humans remains to be determined.In the ...

Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: review of published reports

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