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Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit--the role of renal replacement therapy.

Naka T, Bellomo R - Crit Care (2004)

Bottom Line: However, if lactate-based dialysate or replacement fluid are used, then in some patients hyperlactatemia results, which decreases the strong ion difference and induces an iatrogenic metabolic acidosis.These effects can be achieved in any patient irrespective of whether they have acute renal failure, because of the overwhelming effect of plasma water exchange on nonvolatile acid balance.Critical care physicians must understand the nature, origin, and magnitude of alterations in acid-base status seen with acute renal failure and during continuous hemofiltration if they wish to provide their patients with safe and effective care.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

ABSTRACT
Acid-base disorders are common in critically ill patients. Metabolic acid-base disorders are particularly common in patients who require acute renal replacement therapy. In these patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid-base status using the Stewart-Figge methodology shows that these patients have greater acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly secondary to hyperphosphatemia, hyperlactatemia, and the accumulation of unmeasured anions. Once continuous hemofiltration is started, profound changes in acid-base status are rapidly achieved. They result in the progressive resolution of acidemia and acidosis, with a lowering of concentrations of phosphate and unmeasured anions. However, if lactate-based dialysate or replacement fluid are used, then in some patients hyperlactatemia results, which decreases the strong ion difference and induces an iatrogenic metabolic acidosis. Such hyperlactatemic acidosis is particularly marked in lactate-intolerant patients (shock with lactic acidosis and/or liver disease) and is particularly strong if high-volume hemofiltration is performed with the associated high lactate load, which overcomes the patient's metabolic capacity for lactate. In such patients, bicarbonate dialysis seems desirable. In all patients, once hemofiltration is established, it becomes the dominant force in controlling metabolic acid-base status and, in stable patients, it typically results in a degree of metabolic alkalosis. The nature and extent of these acid-base changes is governed by the intensity of plasma water exchange/dialysis and by the 'buffer' content of the replacement fluid/dialysate, with different effects depending on whether lactate, acetate, citrate, or bicarbonate is used. These effects can be achieved in any patient irrespective of whether they have acute renal failure, because of the overwhelming effect of plasma water exchange on nonvolatile acid balance. Critical care physicians must understand the nature, origin, and magnitude of alterations in acid-base status seen with acute renal failure and during continuous hemofiltration if they wish to provide their patients with safe and effective care.

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Related in: MedlinePlus

Effect of high-volume hemofiltration (HVHF) on chloride, effective strong ion difference (SIDe), and strong ion gap (SIG).
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Figure 9: Effect of high-volume hemofiltration (HVHF) on chloride, effective strong ion difference (SIDe), and strong ion gap (SIG).

Mentions: Recently, HVHF was applied to the treatment of septic shock patients, with favorable hemodynamic results [24]. However, if commercial lactate-buffered replacement fluid is used during HVHF, then patients might receive more than 270 mmol/hour exogenous lactate. This lactate load could overcome endogenous lactate metabolism, even in healthy subjects [25], and result in progressive hyperlactatemia. Hyperlactatemia has been reported with lactate-buffered fluids in critically ill ARF patients treated with intermittent hemofiltration and a lactate load of 190–210 mmol/hour [16]. Such hyperlactatemia might induce a metabolic acidosis. Cole and coworkers [26] studied the effect of HVHF on acid–base balance. HVHF with lactate-buffered replacement fluids (6 l/hour of lactate-buffered fluids) induced iatrogenic hyperlactatemia. Plasma lactate levels increased from a median of 2.51 mmol/l to a median of 7.3 mmol/l at 2 hours (Fig. 8). This change was accompanied by a significant decrease in bicarbonate and base excess. However, such hyperlactatemia had only a mild and transient acidifying effect. A decrease in chloride and effective SID and the removal of unmeasured anions (decrease in SIG) all rapidly compensated for this effect (Fig. 9). Thus, the final effect was that HVHF induced only a minor change in pH from 7.42 to 7.39 at 2 hours. In the period from 2 to 8 hours, the blood lactate concentration remained stable at around 7–8 mmol/l, whereas compensatory effects continued, which restored bicarbonate levels to 27.2 mmol/l and pH to 7.44 by 8 hours of treatment.


Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit--the role of renal replacement therapy.

Naka T, Bellomo R - Crit Care (2004)

Effect of high-volume hemofiltration (HVHF) on chloride, effective strong ion difference (SIDe), and strong ion gap (SIG).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC420038&req=5

Figure 9: Effect of high-volume hemofiltration (HVHF) on chloride, effective strong ion difference (SIDe), and strong ion gap (SIG).
Mentions: Recently, HVHF was applied to the treatment of septic shock patients, with favorable hemodynamic results [24]. However, if commercial lactate-buffered replacement fluid is used during HVHF, then patients might receive more than 270 mmol/hour exogenous lactate. This lactate load could overcome endogenous lactate metabolism, even in healthy subjects [25], and result in progressive hyperlactatemia. Hyperlactatemia has been reported with lactate-buffered fluids in critically ill ARF patients treated with intermittent hemofiltration and a lactate load of 190–210 mmol/hour [16]. Such hyperlactatemia might induce a metabolic acidosis. Cole and coworkers [26] studied the effect of HVHF on acid–base balance. HVHF with lactate-buffered replacement fluids (6 l/hour of lactate-buffered fluids) induced iatrogenic hyperlactatemia. Plasma lactate levels increased from a median of 2.51 mmol/l to a median of 7.3 mmol/l at 2 hours (Fig. 8). This change was accompanied by a significant decrease in bicarbonate and base excess. However, such hyperlactatemia had only a mild and transient acidifying effect. A decrease in chloride and effective SID and the removal of unmeasured anions (decrease in SIG) all rapidly compensated for this effect (Fig. 9). Thus, the final effect was that HVHF induced only a minor change in pH from 7.42 to 7.39 at 2 hours. In the period from 2 to 8 hours, the blood lactate concentration remained stable at around 7–8 mmol/l, whereas compensatory effects continued, which restored bicarbonate levels to 27.2 mmol/l and pH to 7.44 by 8 hours of treatment.

Bottom Line: However, if lactate-based dialysate or replacement fluid are used, then in some patients hyperlactatemia results, which decreases the strong ion difference and induces an iatrogenic metabolic acidosis.These effects can be achieved in any patient irrespective of whether they have acute renal failure, because of the overwhelming effect of plasma water exchange on nonvolatile acid balance.Critical care physicians must understand the nature, origin, and magnitude of alterations in acid-base status seen with acute renal failure and during continuous hemofiltration if they wish to provide their patients with safe and effective care.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

ABSTRACT
Acid-base disorders are common in critically ill patients. Metabolic acid-base disorders are particularly common in patients who require acute renal replacement therapy. In these patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid-base status using the Stewart-Figge methodology shows that these patients have greater acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly secondary to hyperphosphatemia, hyperlactatemia, and the accumulation of unmeasured anions. Once continuous hemofiltration is started, profound changes in acid-base status are rapidly achieved. They result in the progressive resolution of acidemia and acidosis, with a lowering of concentrations of phosphate and unmeasured anions. However, if lactate-based dialysate or replacement fluid are used, then in some patients hyperlactatemia results, which decreases the strong ion difference and induces an iatrogenic metabolic acidosis. Such hyperlactatemic acidosis is particularly marked in lactate-intolerant patients (shock with lactic acidosis and/or liver disease) and is particularly strong if high-volume hemofiltration is performed with the associated high lactate load, which overcomes the patient's metabolic capacity for lactate. In such patients, bicarbonate dialysis seems desirable. In all patients, once hemofiltration is established, it becomes the dominant force in controlling metabolic acid-base status and, in stable patients, it typically results in a degree of metabolic alkalosis. The nature and extent of these acid-base changes is governed by the intensity of plasma water exchange/dialysis and by the 'buffer' content of the replacement fluid/dialysate, with different effects depending on whether lactate, acetate, citrate, or bicarbonate is used. These effects can be achieved in any patient irrespective of whether they have acute renal failure, because of the overwhelming effect of plasma water exchange on nonvolatile acid balance. Critical care physicians must understand the nature, origin, and magnitude of alterations in acid-base status seen with acute renal failure and during continuous hemofiltration if they wish to provide their patients with safe and effective care.

Show MeSH
Related in: MedlinePlus