To the Editor:—

The report by Scheingraber et al.  1highlights the phenomenon of acidemia after infusion of 0.9% saline in the perioperative period. The accompanying editorial 2discusses several relevant points; however, we are disappointed that neither the article nor the editorial addresses the central issue of the relative merits of the Stewart approach 3in describing acid–base physiology and pathophysiology.

Compared with the Henderson-Hasselbalch approach, the Stewart approach has a number of appealing features. (1) The control of acid–base and water homeostasis can be explained in terms of both sodium and chloride regulation. (2) Acid–base status is partly controlled by a number of plasma electrolytes, notably sodium and chloride. These electrolytes can be manipulated in the clinical setting to optimize acid-base status. (3) The factors controlling acid–base status are independent. Criticisms of the Henderson-Haselbalch approach include a lack of independence between carbon dioxide and bicarbonate. 4(4) The Henderson-Hasselbalch approach does not allow assessment of nonvolatile buffers, whereas the Stewart approach explicitly includes assessment of weak acids. 4 

Comparison of the Stewart and Henderson-Hasselbalch approaches is complicated by the fact that both approaches adequately describe the acid–base end point, as Scheingraber et al.  demonstrate. 1Further study is required to determine which approach better describes the mechanisms of acid–base physiology.

Previous animal studies 5have suggested that the alkalinizing effect of lactate-containing solutions in acute resuscitation is time dependent, which underscores the concept of lactate as a strong ion. The removal of lactate from the circulation will increase the strong ion difference and reduce acidosis. 3This effect may be supplemented by further increases in the strong ion difference associated with lactate metabolism 6; in contrast, added chloride ions appear to persist longer in the circulation. Subsequently, a smaller strong ion difference is maintained along with greater acidosis, as seen in the report by Scheingraber et al.  1 

References

1.
Scheingraber S, Rehm M, Sehmisch C, Finsterer U: Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. A NESTHESIOLOGY 1999; 90:1265–70
2.
Prough DS, Bidani A: Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline (editorial). A NESTHESIOLOGY 1999; 90:1247–9
3.
Stewart PA: Modern quantitative acid-base chemistry. Can J Physiol Pharmacol 1983; 61:1444–61
4.
Fencl V, Leith DE: Stewart’s quantitative acid-base chemistry: Applications in biology and medicine. Respir Physiol 1993; 91:1–16
5.
Traverso LW, Lee WP, Langford MJ: Fluid resuscitation after an otherwise fatal hemorrhage: I Crystalloid solutions. J Trauma 1986; 26:168–75
6.
White SA, Goldhill DR: Is Hartmann’s the solution? Anaesthesia 1997; 52:422–7.