Perspectives on the Predictive Role of PvCO2 × Ve/Q for Hyperlactatemia During Cardiopulmonary Bypass

To the Editor, We read with great interest the article by Kowara et al.,[1] which highlights the potential of PvCO2 × Ve/Q as a key predictive marker for hyperlactatemia during cardiopulmonary bypass (CPB). This study is an important step toward identifying reliable, real-time markers for monitoring hypoperfusion. However, several critical aspects of this work deserve further discussion. The authors show that PvCO2 × Ve/Q predicts lactate kinetics with high sensitivity, though its specificity (55.6%) is modest. This raises the risk of false-positive alerts, leading to unnecessary interventions during CPB. To improve accuracy, combining PvCO2 × Ve/Q with other parameters like oxygen extraction ratio or respiratory quotient could enhance its clinical value.[2,3] Continuous monitoring of PvCO2 × Ve/Q instead of intermittent sampling could provide dynamic assessments and support real-time decisions. The study’s exclusion criteria such as preoperative lactate levels >2 mmol/L and pump flow indices outside 1.2–2.4 L/min/m² limits its generalizability. Patients undergoing CPB often have comorbidities and suboptimal perfusion. Future studies should evaluate PvCO2 × Ve/Q in broader clinical settings, including extreme conditions like profound hypothermia, prolonged CPB, or the use of vasopressors and blood transfusions, which could affect CO2 and lactate levels and warrant further analysis.[4] The use of PvCO2 from the CPB circuit introduces another consideration as it may be affected by oxygenator efficiency and mechanical ventilation settings, potentially confounding its link with lactate levels. Future studies should address these variables to ensure the reliability of PvCO2 as a marker. Preoperative variability in acid-base status and systemic physiology, such as baseline metabolic conditions, acidemia, or alkalemia may influence PvCO2 and lactate metabolism. Accounting for these factors may enhance its clinical utility. While PvCO2 × Ve/Q is presented as a surrogate for anaerobic metabolism, further research on its relationship with systemic inflammatory response such as complement activation and cytokine release during CPB could determine, whether it reflects localized hypoperfusion, global metabolic derangements, or both. Although VCO2 was mentioned as a potential predictor of lactate levels, its role was overshadowed by the focus on PvCO2 × Ve/Q. Comparing these metrics could help determine their relative importance in detecting hypoperfusion. The specificity of PvCO2 × Ve/Q as a marker for hypoperfusion needs to be investigated. Changes in PvCO2 × Ve/Q might also result from ventilation-perfusion mismatches unrelated to perfusion deficits. Distinguishing these scenarios is crucial for avoiding misinterpretation of the data. A direct comparison of PvCO2 × Ve/Q with established markers, such as the arterial-to-venous CO2 difference or lactate clearance rates would contextualize its relative efficacy and provide a stronger foundation for its integration into clinical practice. The study briefly addresses the limitations of SvO2 as a standalone marker for hypoperfusion during CPB but does not explore the potential synergy of combining PvCO2 × Ve/Q with other real-time monitoring modalities like near-infrared spectroscopy.[5] Integrating these approaches may allow for earlier recognition of perfusion deficits and reduce postoperative complications. In conclusion, Kowara et al. have contributed valuable insights into the predictive role of PvCO2 × Ve/Q for hyperlactatemia during CPB. However, further studies are needed to validate its specificity, examine its utility in diverse patient populations, and assess its integration with other monitoring tools. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.