Aim: Cardiogenic shock (CS) remains a clinical challenge with a high mortality risk. Mechanical circulatory support (MCS) could improve outcomes via hemodynamic stabilization, but is linked to a high mortality risk, and should therefore only be used if conventional treatment fails. The aim of this study was to evaluate lactate and lactate kinetics for the early identification of patients with deteriorating CS. 

Methods: Data of patients with CS and two lactate measurements within 90 minutes after presentation from a tertiary care hospital between 2009 and 2019 were analyzed. Between both lactate measurements, patients received volume therapy, inotropes and vasopressors, and no MCS. Multivariable Cox regression models were fitted to assess the association between baseline lactate as well as lactate kinetics and the primary endpoint of 30-day mortality. The optimal baseline lactate cut-off for the prediction of the primary endpoint was derived by receiver operating characteristic (ROC) curve analysis.

Results: A total of 533 patients were analyzed; mean age was 69 years (interquartile range 59–78) years, 374 (70.3%) were male, 241 (45.6%) presented with CS due to acute myocardial infarction and 328 (61.7%) with cardiac arrest. Baseline lactate was 4.9 (interquartile range 2.6-9.8) mmol/l and increased in 216 (40.5%) of the patients with a median change of -0.1 (interquartile range -1,3-0.8) mmol/l within 90 minutes. 

ROC curve analysis identified a baseline lactate of ≥6.6 mmol/l as the best cut-off value for the prediction of 30-day mortality. A baseline lactate ≥6.6 mmol/l as well as an increase in lactate within 90 minutes were strongly associated with a higher risk of 30-day mortality, even after adjustment for relevant confounders [hazard ratio (HR) 2.77, 95% confidence interval (CI) 2.17-3.55 for baseline lactate ≥6 mmol/l; HR 1.72, 95% CI 1.37-2.16 for an increase in lactate within 90 minutes].

Combining both measures yielded a more granular assessment of the 30-day mortality risk: The 30-day mortality risk of patients with a high baseline lactate was high (30-day mortality 76%, 95% CI 66.82-82.65, in patients with vs. 81.19%, 95% CI 70.74-88.02, in patients without a lactate increase within 90 minutes). In addition, patients with a low baseline lactate and an increase within 90 minutes were at similarly high risk of death at 30 days (65.04%, 95% CI 54.09-73.38) while patients with low initial lactate and stable or declining 90 minutes values were at lower risk of death (37.32%, 95% CI 29.02-44.65; Figure 1). 

Conclusion: In addition to a high baseline lactate concentration, an increase in lactate during the first 90 minutes of CS identifies patients at high risk of death, even in those with low or normal baseline lactate. In patients with low lactate concentrations at admission for cardiogenic shock, an increase in lactate within 90 minutes identifies a high-risk subgroup of patients who may benefit from mechanical circulatory support.