Independent association of lung injury with lactate after pulmonary vascular intervention: a cross-sectional study

Background Postoperative hyperlactatemia is associated with organ dysfunction, but its independent role in lung injury remains underexplored, particularly relative to pulmonary hemodynamics. Objective To determine whether postoperative lactate independently correlates with lung injury after surgery, dissected from pulmonary hemodynamic parameters. Methods In this single-center cross-sectional study, 143 surgical patients (non-injury = 101, injury = 42) were analyzed. Baseline characteristics, pulmonary hemodynamics (SPAP, PVR, TPR), and lactate levels were collected. Univariate and multifactorial logistic regression evaluated risk factors. Additive/multiplicative interactions between lactate and hemodynamic variables were tested using RERI/AP and product-term models. Results Of the 143 patients studied, 42 (29.4%) developed lung injury. Univariate analysis identified that elevated postoperative lactate (≥ 1.97 mmol/L), pulse, systolic pulmonary artery pressure (sPAP), pulmonary vascular resistance (PVR), total pulmonary resistance (TPR), and preoperative CO₂ were significant risk factors for lung injury (all P  < 0.05). In multivariate analysis, postoperative lactate remained an independent predictor of lung injury across all adjusted models (adjusted OR range: 1.915–2.040, all P  < 0.05). Multiplicative interaction analysis revealed a significant interaction between PVR and postoperative lactate (OR = 4.590, 95% CI: 1.098–19.186, P  = 0.037). However, measures of additive interaction (RERI, AP, S) for sPAP, PVR, and TPR with postoperative lactate were not statistically significant. Conclusion Elevated postoperative lactate independently correlates with lung injury without synergistic effects from pulmonary hemodynamic dysfunction. Lactate assessment may provide standalone value for early risk stratification.