Amperometric measurement of lactate

Measurement of glucose (cGlu) and measurement of lactate (cLac) fall with measurement of dissolved oxygen concentration using the Clark electrode into the category of amperometric measurements, the principles of which are discussed in abundant detail elsewhere. As a main reference for this topic, I refer the readers to an excellent overview article by Oleh Smutok.

Furthermore, the function and structure of the glucose electrode is so similar that many of the points raised in that chapter also apply to lactate measurement. In the interest of brevity, that material is not duplicated here.

Structure of the lactate-sensitive electrode

The E7077 lactate electrode in the local unit relies on lactate oxidation by a bacterial lactate oxidase enzyme, which generates a product (hydrogen peroxide) which is more easily reduced than the parent molecule. Lactate itself could also be reduced, but the voltage required for this would be too great, and at such a high voltage the cell would begin to reduce other molecules as well (most notably, water).

The electrode possesses a special multilayer membrane, which is composed of three major components:

• A lactate-permeable outer membrane
• A lactate-oxidising middle layer, rich in lactate oxidase
• A peroxide-permeable inner membrane

The selectivity of the outer membrane and the enzyme are such that one can reliably expect only lactate to be oxidised, to the exclusion of most other molecules. However, the Reference Manual lists a large number of molecules which can potentialy cause interference- notably ascorbic acid, bilirubin, citrate, EDTA, ethanol, heparin, glucose, paracetamol, salicylate and urea. The most famous of these interactions is with glycolic acid, the metabolic product of ethylene glycol metabolism. Glycolic acid also serves as a substrate for lactate oxidase and this gives rises to a spuriously elevated lactate when measured by ABG. The formal laboratory method relies on lactate dehydrogenase, which has far greater lactate specificity and therefor yields a different (accurate) result. This source of error is made famous by its use in a classic ABG question (Question 1.12) from the 2003 edition of Data Interpretation in Intensive Care Medicine by Bala Venkatesh et al. It had also made an appearance in Question 20.2 from the second CICM Fellowship Exam paper of 2017.

Anyway. Inside the membrane, the following events take place:

• Lactate is oxidised into pyruvate, consuming O₂ and producing hydrogen peroxide
• Hydrogen peroxide diffuses into the inner electrolyte, and is reduced at the cathode
• The oxygen produced in this reduction is reused in the ongoing oxidation of lactate

The oxygen dependence of this reaction is discussed in greater detail in the glucose electrode chapter. Suffice to say, a tiny amount of oxygen is required to kickstart the oxidation reaction in the middle chamber, and there should be enough oxygen for this in even the most anoxic sample.

The lactate electrode in the local unit offers a useful range between 0 and 30 mmol/L of lactate, which covers the majority of situations. Though occasionally patients present with a higher lactate than the ABG machine can measure, one can fall back on a certain pragmatic argument. Who cares how much higher than 30mmol/L it is; one's management of severe lactic acidosis will not be substantially different irrespective of whether the lactate is 30mmol/L or 50mmol/L.

Lactic acidosis in its many forms is discussed in the Metabolic Acidosis section.