Short summary: The occurrence of metabolic alkalosis has been described recently in critically ill patients developing hypernatremia. To clarify whether a pure dehydration as cause of hypernatremia contributes to the development of metabolic alkalosis, we dehydrated serum samples of 10 healthy volunteers. Acid–base analysis before and after dehydration showed development of marked metabolic alkalosis by 29 % dehydration.
The development of metabolic alkalosis was described recently in patients with hypernatremia. However, the causes for this remain unknown. The current study serves to clarify whether metabolic alkalosis develops in vitro after removal of free water from plasma and whether this can be predicted by a mathematical model.
Materials and methods
Ten serum samples of healthy humans were dehydrated by 29 % by vacuum centrifugation corresponding to an increase of the contained concentrations by 41 %. Constant partial pressure of carbon dioxide at 40 mmHg was simulated by mathematical correction of pH [pH(40)]. Metabolic acid–base state was assessed by Gilfix’ base excess subsets. Changes of acid–base state were predicted by the physical–chemical model according to Watson.
Evaporation increased serum sodium from 141 (140–142) to 200 (197–203) mmol/L, i.e., severe hypernatremia developed. Acid–base analyses before and after serum concentration showed metabolic alkalosis with alkalemia: pH(40): 7.43 (7.41 to 7.45) vs 7.53 (7.51 to 7.55), p = 0.0051; base excess: 1.9 (0.7 to 3.6) vs 10.0 (8.2 to 11.8), p = 0.0051; base excess of free water: 0.0 (− 0.2 to 0.3) vs 17.7 (16.8 to 18.6), p = 0.0051. The acidifying effects of evaporation, including hyperalbuminemic acidosis, were beneath the alkalinizing ones. Measured and predicted acid–base changes due to serum evaporation agreed well.
Evaporation of water from serum causes concentrational alkalosis in vitro, with good agreement between measured and predicted acid–base values. At least part of the metabolic alkalosis accompanying hypernatremia is independent of renal function.