Introduction
The association of hyperlactataemia and acidosis with worsened clinical outcome has been demonstrated in numerous patient and disease states 12. However, hyper-lactataemia itself has complex origins and is variably associated with acidosis and with patient morbidity and mortality. The latter depends greatly on the origin of lactate production. 'Type A' hyperlactataemia is associated with anaerobic respiration, inadequate tissue oxygen delivery, acidosis, and increased morbidity and mortality 3. 'Type B' hyper-lactataemia occurs in the presence of adequate oxygen delivery with increased substrate utilisation. Differentiation between these aetiologies is important because they represent discrete metabolic processes with differing therapies and prognoses. Hyperlactataemia developing during cardiopulmonary bypass (CPB) is associated with worsened postoperative outcome 4; although 'type A' lactic acidosis is the more commonly cited origin, this has been questioned 5.
Origin of hyperlactataemia during cardiopulmonary bypass
In the previous issue of Critical Care, Ranucci and colleagues report a prospective observational study undertaken to identify the source of hyperlactatemia developing during CPB and its association with outcome 1. Data were analysed to assess independent association between the tested variables and the peak blood lactate concentration. They concluded that hyperlactataemia was more likely during prolonged CPB time, that it was independently associated with low oxygen delivery, that it was almost invariably associated with hyper-glycaemia, and that it was a predictor of worse postoperative morbidity (although not mortality).
The association with low oxygen delivery is suggestive that this underlies the mechanism for 'type A' hyperlactataemia, but is not conclusive. Reduced oxygen delivery is compatible with aerobic respiration if oxygen consumption is simultaneously decreased. Increased endogenous catecholamine production during times of such 'stress' stimulates increased blood glucose concentrations and glycolysis 6, with a resultant increase in lactate production due to 'flooding' of pyruvate dehydrogenase 7. This is not an acidifying process because it develops under aerobic conditions; it has been termed 'stress hyperlactataemia' 8. The presence or absence of acidosis is therefore an important mechanism for separating the aerobic and anaerobic aetiologies of hyperlactataemia.
In Ranucci's study 1, base excess was maintained within a normal range during CPB by administrating bicarbonate solution. No association can therefore be made between the presence of hyperlactataemia and that of acidosis. This information may be available in surrogate form as the dose of bicarbonate required to maintain normal base excess levels in patients with or without hyperlactataemia. If the dose requirement for bicarbonate is significantly higher in the hyperlactataemia group, then the presence of 'type A' lactic acidosis can be inferred. However, if the bicarbonate requirements are the same, it raises the possibility that this is stress-induced 'type B' hyperlactataemia. Another marker that can separate the anaerobic and aerobic aetiologies of raised lactate is the lactate:pyruvate ratio. Under aerobic conditions with stimulated glycolysis, pyruvate synthesis increases in proportion to lactate, giving a normal lactate:pyruvate ratio of 10:1. However, once anaerobic conditions develop, lactate increases at a rate in excess of that for pyruvate, with a resultant increase in their ratio 9. The presence of an increased lactate:pyruvate ratio in association with acidosis, low oxygen delivery and hyperlactataemia during CPB would be conclusive evidence that inadequate oxygen delivery and anaerobic mechanisms are predominating.