Stewart's physicochemical approach in neurosurgical patients with hyperchloremic metabolic acidosis during propofol...

There is both in vitro and clinical evidence that high-dose propofol can inhibit mitochondrial respiration, resulting in metabolic acidosis. The purpose of this study was to evaluate the effects of propofol anesthesia on the acid-base status in neurosurgical patients with large amount of normal saline administration. Thirty patients undergoing clipping of cerebral aneurysm were randomly assigned to receive propofol (n=15) or isoflurane (n=15). Propofol dose (mean+/-standard error) infused for maintenance was 5.7+/-0.2 mg/kg/h in propofol group. Acid-base parameters such as PaCO2, pH, serum bicarbonate concentration, standard base excess, serum electrolyte concentration, total protein, albumin, lactate, and phosphate were measured before and 4 hours after the induction of anesthesia, and after surgery. The apparent strong ion difference (SIDa), the effective SID (SIDe), and the amount of weak plasma acid were calculated using the Stewart equation. There were no significant differences in pH, PaCO2, bicarbonate, and lactate between 2 groups throughout the whole investigation period. After surgery, standard base excess significantly decreased in both groups without intergroup difference. SIDa and SIDe significantly decreased in both groups, and lactate and strong ion gap significantly increased after surgery in propofol group, but there were no significant differences between 2 groups. Both propofol and isoflurane were associated with hyperchloremic metabolic acidosis in neurosurgical patients with large amount of normal saline administration. The acid-base balance between the 2 anesthetics was similar using Stewart's physicochemical approach.