High End-Surgery Arterial Lactate Concentration (ES-ALC) predicts poor outcome after hepatectomy. The aim of this study was to identify intraoperative hemodynamic parameters predicting high ES-ALC during elective liver resection. Patients who underwent liver resection between 2017 and 2018, under FloTrac/EV1000^TM hemodynamic monitoring, were included. The ES-ALC cutoff best predicting severe postoperative complications was identified. Association between high ES-ALC and preoperative and intraoperative variables was assessed. 108 patients were included; 90-day mortality was 0.9% and severe morbidity 14.8%. ES-ALC cutoff best discriminating severe complications was 5.05 mmol/L. Patients with ES-ALC > 5.0 mmol/L had a relative risk of severe complications of 2.8% (p = 0.004). High ES-ALC patients had longer surgery and ischemia duration, larger blood losses and higher requirements of fluids and blood transfusions. During surgery, hemoglobin concentration and oxygen delivery (DO₂) decreased more significantly in patients with high ES-ALC, although they had similar values of stroke volume and cardiac output to those of other patients. At multivariate analysis, surgery duration and lowest recorded DO₂ value were the strongest predictors of high ES-ALC. ES-ALC > 5.0 mmol/L in elective liver resection predicts postoperative morbidity and is essentially driven by the impaired DO_2. Timely correction of blood losses might prevent the ES-ALC increase.

Background: Intraoperative fluid management based on pulse pressure variation has shown potential to reduce postoperative pulmonary complications (PPCs) and improve clinical outcomes in various surgical settings. However, its efficacy and safety have not been assessed in patients undergoing thoracic surgery with one-lung ventilation. Methods: Patients scheduled for pulmonary lobectomy using uniportal video-assisted thoracic surgery approach were randomly assigned to two groups. In the PPV group, fluid administration was guided by the pulse pressure variation parameter, while in the near-zero group, it was guided by conventional hemodynamic parameters. The primary outcome was the partial pressure of oxygen (PaO₂)/ fraction of inspired oxygen (FiO₂) ratio 15 min after extubation. The secondary outcomes included extubation time, the incidence of postoperative pulmonary complications in the first three postoperative days, and the length of hospital stay. Results: The PaO₂/FiO₂ ratio did not differ between the two groups (364.48 ± 38.06 vs. 359.21 ± 36.95; p = 0.51), although patients in the PPV group (n = 44) received a larger amount of both crystalloids (1145 ± 470.21 vs. 890 ± 459.31, p = 0.01) and colloids (162.5 ± 278.31 vs 18.18 ± 94.68, p = 0.002) compared to the near-zero group (n = 44). No differences were found in extubation time, type and number of PPCs, and length of hospital stay. Conclusions: PPV-guided fluid management in thoracic surgery requiring one-lung ventilation does not improve pulmonary gas exchange as measured by the PaO₂/FiO₂ ratio and does not seem to offer clinical benefits. Additionally, it results in increased fluid administration compared to fluid management based on conventional hemodynamic parameters.

Background: Intraoperative hypotension during major abdominal surgery is common and can result from changes in preload, afterload, or myocardial contractility. Recognising the underlying cause is essential for targeted haemodynamic management. Arterial dP/dt_max has been proposed as a surrogate marker for ventricular systolic function, but its behaviour during fluid and vasopressor administration under general anaesthesia remains not fully understood. This study evaluated changes in radial arterial dP/dt_max following protocol-guided fluid administration and norepinephrine boluses during intraoperative hypotension. Methods: This prospective observational study involved 88 adult patients undergoing elective major abdominal surgery with continuous radial arterial waveform monitoring. Hypotensive episodes were defined as a mean arterial pressure <65 mmHg persisting for at least 60 s and were managed according to a predefined algorithm based on stroke volume variation and dynamic arterial elastance. The primary outcome was the change in arterial dP/dt_max from baseline to 5 min after fluid administration. Linear mixed-effects models were used to account for repeated intervention episodes within patients. Results: A total of 502 protocol-guided intervention episodes contributed by 76 patients were included in the primary analysis: 228 fluid-treated episodes and 274 norepinephrine-treated episodes. Estimated mean arterial dP/dt_max increased from 517 mmHg·s⁻¹ (95% CI 477–557) at baseline to 631 mmHg·s⁻¹ (95% CI 591–671) at 5 min during fluid-treated episodes and from 575 mmHg·s⁻¹ (95% CI 536–615) to 647 mmHg·s⁻¹ (95% CI 608–686) during norepinephrine-treated episodes (both p < 0.001). A significant intervention-condition-by-time interaction was observed (F = 5.55, p = 0.019), indicating that temporal evolution of arterial dP/dt_max differed between the two algorithm-defined haemodynamic conditions. Conclusions: Radial arterial dP/dt_max increased after both fluid administration and norepinephrine, confirming its sensitivity to haemodynamic loading conditions. It should therefore be interpreted as an integrated haemodynamic variable influenced by ventricular performance, preload, and arterial properties rather than as a direct measure of intrinsic myocardial contractility.