Lactate clearance in cardiogenic shock: can it help guide therapy and outcome?

Abstract Introduction Lactate is a marker of unmet metabolic demand, and blood levels may be increased in many disease states, including cardiogenic shock. Lactate measurement has been used to guide diagnosis, resuscitation, and prognostication. It remains a non-specific biomarker and elevated lactate levels can have multiple causes, including as part of normal physiology. Lactate metabolism and clearance is around 70-75% hepatic and 25-30% renal. (1) The role of lactate in cardiogenic shock (CS) is complex. Cardiac myocytes use lactate as an energy source, at the same time as expressing endogenous lactate. (2) Studies have shown an association between elevated lactate and increased mortality in CS. However, no reliable timepoint or lactate plasma level at which mortality increases have been defined (3). We tested the hypothesis that lactate clearance in CS over time may be a more reliable prognostic marker than absolute levels (4). Methods 79 patients admitted to the cardiac catheterisation laboratories at our institution for primary percutaneous coronary intervention with Society of Cardiovascular Angiography and Interventions (SCAI) class D or E CS had serial lactate measurements taken on admission, on arrival at the intensive care unit (ICU), and then at 6 hours, 12 hours and 18 hours after ICU admission to calculate clearance (defined as % reduction from baseline). None of the patients received mechanical circulatory support (MCS) at any point. Patients were divided into those who survived to ICU discharge and those who died during ICU admission. Statistical analysis was performed using Medcalc with Kruskal-Wallis analysis. Results Out of 79 patients admitted, 46 (58.2%) died during ICU admission and 33 (41.8%) survived to ICU discharge. Lactate values were significantly higher in non-survivors at all timepoints (Table 1), however there was overlap in lactate levels between groups, not allowing definition of a cut-off level for mortality. There was no statistically significant difference in lactate clearance between groups at ICU admission, 6 hours and 12 hours. This turned significant at 18 hours (Table 1). Conclusion This study shows that patients with SCAI class D or E CS who did not survive ICU admission had similar lactate clearance for the first 12 hours, which subsequently dropped off between 12 and 18 hours when compared to survivors. There appears to be an inflection point between 12 - 18 hours after ICU admission, where lactate clearance has the potential to serve as a biomarker to demarcate survivors from non-survivors. In extension, this may provide useful guidance when considering establishing patients on MCS. The 12-hour window provides time to ensure that MCS is appropriate and that the right patient receives the right device.