Written by Clay Smith
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Hyperlactatemia appears to arise from impaired oxygen utilization more often than decreased O2 delivery but doesn’t cause acidemia unless there is impaired renal function. The novel “alactic base excess” may give us an early way to tell when the kidneys are failing to compensate.
Why does this matter?
Increasingly, lactate is viewed as a normal byproduct of glucose metabolism, metabolized to CO2 and water unless lactate production exceeds oxidative capacity, not as a byproduct of anaerobic metabolism. The authors hypothesized that, “hyperlactatemia is present both at high and low values of ScvO2 and that the presence or absence of kidney injury will determine the final effect of plasma lactate concentration on pH.”
This gives my brain lactic acidosis…or does it
The authors did a post-hoc analysis on 1,741 patients with severe sepsis or septic shock in the ALBIOS trial; all had paired ScvO2 and lactate. Lactate may come from decreased O2 delivery (35% – low ScvO2) or decreased utilization (65% – normal or high ScvO2). As an acid and strong ion, it should lower the pH, but it usually doesn’t with normal renal function. Once the kidneys can’t clear the other fixed acids (phosphoric, sulfuric, etc.) which are strong ions, acidemia ensues. The alactic base excess* is a way to estimate renal compensation in septic patients.
From cited article: SID, strong ion difference.
What are the clinical implications?
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A standard amount of fluid for all septic patients may not be helpful for most, as the issue is often not a macrocirculatory defect in oxygen delivery, rather utilization of oxygen by the tissues.
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In this study, lactate was not associated with acidosis unless there was impaired renal function.
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The authors suggest, “patients might be first stratified on the basis of ScvO2 to understand the origin of lactate production, and then on the basis of the alactic BE to better understand organ (i.e., kidney) perfusion and volemia. Changes in this simple parameter over time may facilitate early restoration of appropriate fluid balance and/or prompt the use of renal replacement therapy.”
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I am hesitant about anything too prescriptive, as we have seen that goal directed therapy has no benefit over standard resuscitation.
Source
Understanding Lactatemia in Human Sepsis: Potential Impact for Early Management. Am J Respir Crit Care Med. 2019 Apr 15. doi: 10.1164/rccm.201812-2342OC. [Epub ahead of print]
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*The novel “alactic base excess” is a way to determine the degree of renal compensation for the acid base disorder. If you have a chance to read this article and Online Supplement in full, it is a lactate pathophysiology tour de force.
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For background:
Base excess (BE) = actual buffer base – ideal buffer base.
Ideal buffer base at pH 7.4 is 42mmol/L. -
They computed a standard BE, as they thought it better represented the buffer base of the extracellular fluid. It is:
Standard BE (mmol/L) = (HCO3 mmol/L – 24.8 mmol/L) + 16.2 mmol/L*(pH – 7.4) -
The “alactic BE” is the sum of the standard BE and lactate:
Alactic BE = standard BE (mmol/L) + lactate (mmol/L)
– A negative value is seen with renal dysfunction and indicates the presence of accumulating fixed acids other than lactate in the plasma, such as sulphuric or phosphoric.
– A value of zero means the acidemia is fully explained by the lactate.
– A positive value indicates the kidney fully compensated for the acidosis, or other mechanisms contributed to metabolic alkalosis (i.e.contraction alkalosis).
