The effect of continuous hemofiltration on acid-base physiology

Continuous hemofiltration techniques have a powerful effect on acid-base physiology. In patients with metabolic acidosis, hemofiltration techniques replace plasma water, which is low in bicarbonate concentration, with a solution, which contains either an above-normal bicarbonate concentration or a high concentration of a multi-carbon anion (lactate or acetate). Such anions are then transformed into CO₂ which is removed by ventilation. This exchange contributes to the correction of acidosis. The conventional view of such changes in acid-base balance is that lactate and acetate correct acidosis by generating bicarbonate. An emerging view, however, is that such oxidizable anions probably alkalinize plasma by increasing the so-called strong ion difference in plasma water. An increase in the strong ion difference (cations - anions) then results in decreased plasma water dissociation and decreased hydrogen ion activity (Stewart's approach). If such oxidizable anions are not fully taken up by the liver and, therefore, remain in plasma water, their ability to correct acidosis is lost. They accumulate in blood and fail to decrease the strong ion difference adequately, resulting in acidosis. This effect (iatrogenic hyperlactatemia with acidification of plasma water) is typically best seen in patients with liver failure. In such patients, bicarbonate-based replacement fluids or dialysate must be used to avoid uncontrolled metabolic acidosis. In addition, the effect of lactate-based replacement fluid on blood lactate concentration can be diagnostically confusing in septic patients with lactic acidosis. In these patients, the iatrogenic increase in lactate makes it very difficult to evaluate the effects of other therapies on the evolution of endogenous lactic acidosis. On the other hand, it appears that lactate clearance through the hemofilter is small compared to endogenous clearance. Accordingly, a falling lactate level in the setting of the recent initiation of hemofiltration is best interpreted as an actual improvement in the patient's acid-base status. Clearly, the effects of hemofiltration on acid-base physiology need to be appreciated and understood if the intensive care physician is to avoid incorrect interpretations of the patient's clinical progress and the consequences of misdirected therapeutic interventions.