According to the approach proposed by Stewart, changes in hydrogen ion (H+) concentration in blood plasma result from water dissociation and its determinants can be reduced to three: the strong ion difference (SID), partial pressure of carbon dioxide (PCO2), and weak acid concentration (ATOT). The SID corresponds to the net charge balance of all strong ions present in plasma. Four defense mechanisms counteract daily acid load: transport of ions across cell membranes, removal of volatile acid (CO2) by the lungs, elimination of ions by the kidney and metabolism by the liver. In renal failure, the mechanisms for non-volatile acid excretion by the kidney are reduced. A hyperchloremic metabolic acidosis develops and is followed by a high anion gap acidosis. In end-stage renal disease, metabolic acidosis has several detrimental effects: enhanced protein degradation, bone demineralization, progression of hyperparathyroidism, and insulin resistance. In the acute setting, metabolic acidosis is also associated with depressed myocardial contractility, arrhythmias, and altered response to vasopressors and drugs. Dialysis therapy can be viewed as an alkalinizing process. The serum bicarbonate concentration achieved can be expected to be different in intermittent hemodialysis versus continuous modalities, such as peritoneal dialysis or continuous renal replacement therapy, since the alkalinizing process is applied over a very different time frame. With intermittent hemodialysis, the post-treatment serum bicarbonate concentration will depend on the dialysis prescription, the choice and dialysance of the buffer base, the concentration gradient of ions across the dialyzer membrane, as well as the patient’s characteristics. Acetate has been largely replaced by bicarbonate, which ameliorates tolerance to intermittent hemodialysis. The SID of the final dialysate used for intermittent hemodialysis is nearly 40 mmol/L, thus very close to the apparent SID of blood plasma of a normal individual. Therefore, hemodialysis can temporarily correct the reduced SID of renal failure. Variants of hemodialysis combining convective and diffusive exchange processes, such as hemodiafiltration and acetate-free biofiltration, are usually considered more potent in regard to correction of renal acidosis; however, the composition of substitution fluids must be physiological and close to the SID of normal plasma. The impact of continuous renal replacement therapy (CRRT) on the acid-base balance of critically ill patients is also determined by several factors: underlying acid-base disorders and severity, types of organ dysfunction, degree of protein catabolism enhancing acid production, and CRRT prescription itself. As much as 750 mmol of bicarbonate could be lost daily during CRRT, requiring the exogenous replacement of as much as 30 mmol/h. In any case, the rate of bicarbonate or “bicarbonate equivalent” administration must exceed the rate of endogenous bicarbonate lost in the effluent to correct metabolic acidosis or to prevent its development. The solutions used for dialysate or replacement fluids may contain lactate, bicarbonate, or citrate as the main anion. Lactate-based solutions are usually well tolerated, but hyperlactatemia may be induced in patients with severe hepatic failure or profound hypoxia. Bicarbonate-based solutions, although routinely used in Europe, are not yet widely available; they are potentially advantageous from a hemodynamic standpoint, and may allow an improved control of the metabolic acidosis.
Maisonneuve-Rosemont Hospital, Affiliated to the University of Montreal, Montreal, Canada
Correspondence to Martine Leblanc, MD, Nephrology and Intensive Care Departments, Maisonneuve-Rosemont Hospital, 5415 de l’Assomption, Montreal, PQ, Canada; e-mail: firstname.lastname@example.org