Serial lactate measurements could provide clinically useful prognostic information in patients with cardiogenic shock.
In a review, investigators synthesized evidence on the pathophysiology, prognostic value, and clinical interpretation of serum lactate in patients with cardiogenic shock. They examined findings from clinical trials, registries, observational studies, and studies involving temporary mechanical circulatory support, including venoarterial extracorporeal membrane oxygenation (VA-ECMO).
Across the studies reviewed, admission lactate was consistently associated with shock severity and mortality. The investigators noted that lactate thresholds of approximately 3 to 3.5 mmol/L identified patients at higher risk of short-term mortality, while one large study of acute myocardial infarction–related cardiogenic shock found that a baseline lactate level of 5 mmol/L provided the optimal cutoff for predicting 30-day mortality.
However, the investigators emphasized that the prognostic value of a single lactate measurement could diminish once treatment has begun. Evidence summarized during the review suggested that serial monitoring could better reflect metabolic recovery and response to therapy.
In a substudy of the IABP-SHOCK II trial found that lactate measured 8 hours following presentation of cardiogenic shock predicted 30-day mortality more accurately than either baseline lactate or lactate clearance. An 8-hour lactate threshold of 3.1 mmol/L following initial management provided the best discrimination for early risk stratification.
The investigators summarized findings showing that reductions in lactate during the first 12 to 24 hours following presentation were consistently associated with improved survival. In a post hoc analysis of the DOREMI trial, complete lactate clearance emerged as the strongest predictor of survival among lactate-derived measures. This prognostic association strengthened over time, with the greatest predictive value observed at 24 hours.
The findings were similar among patients receiving mechanical circulatory support. According to the investigators, preimplantation lactate levels in patients receiving VA-ECMO reflected disease severity and were incorporated into several prognostic scoring systems. Following VA-ECMO initiation, early lactate clearance was among the strongest predictors of survival, whereas persistent hyperlactatemia despite adequate device flow was associated with multiorgan failure and poor outcomes.
The investigators also highlighted evidence from a post hoc analysis of the HYPO-ECMO study, which found that a secondary lactate peak during the first 7 days following VA-ECMO initiation occurred in approximately 24% of patients and was independently associated with poorer outcomes.
Elevated lactate concentrations in cardiogenic shock may arise through multiple mechanisms, according to the investigators. Reduced cardiac output and systemic hypoperfusion contribute to anaerobic lactate production, but adrenergic stimulation, post–cardiac arrest syndrome, ischemia-reperfusion injury, systemic inflammation, mitochondrial dysfunction, and impaired hepatic or renal clearance may also increase lactate levels.
These mechanisms may complicate clinical interpretation. The investigators cited evidence showing that epinephrine was associated with substantially higher lactate concentrations compared with norepinephrine or dobutamine in patients with acute myocardial infarction–related cardiogenic shock, supporting the role of catecholamine-driven lactate production independent of tissue hypoxia. Conversely, chronic beta-blocker therapy may blunt lactate elevations, potentially leading physicians to underestimate shock severity if lactate is considered in isolation.
The review had limitations inherent to its design. As a narrative review, it synthesized evidence from heterogeneous sources, including observational studies, registries, randomized trials, and post hoc analyses. The investigators noted that lactate values should be interpreted within the broader clinical context and not used as standalone measures of treatment success, treatment failure, or futility.
“[L]actate should be interpreted as an integrative and dynamic biomarker reflecting the balance between hypoperfusion, metabolic stress, and clearance rather than tissue hypoxia alone,” wrote lead study author Bruno Levy, MD, of Université de Lorraine and Centre Hospitalier Régional Universitaire de Nancy in France, and colleagues. They added that trajectory-based lactate assessment may provide important information for risk stratification, therapeutic guidance, and evaluation of shock reversibility.
Dr. Levy reported relationships with AOP Orphan Pharmaceuticals GmbH and Viatris. The study authors reported no other competing interests.
Source: Annals of Intensive Care