Background Microcirculatory dysfunction may persist despite restoration of conventional macrocirculatory targets in sepsis, reflecting loss of hemodynamic coherence. This review synthesizes current microcirculatory monitoring approaches according to the physiological information they provide and examines how complementary modalities may be integrated to characterize persistent or regional tissue hypoperfusion. Main body A narrative review of PubMed-indexed literature was conducted, with emphasis on bedside peripheral perfusion assessment, tissue oxygenation and superficial perfusion imaging, direct microvascular visualization, and organ- or tissue-specific monitoring. Recent studies were prioritized together with landmark methodological and validation studies. Available techniques interrogate distinct but overlapping components of the circulation. Bedside peripheral measures provide rapid information on skin reperfusion and vascular tone; spectroscopic and optical techniques characterize tissue oxygenation, reactivity, and spatial perfusion heterogeneity; direct microvascular imaging enables assessment of microvascular density and flow; and organ-specific approaches provide information on renal, cerebral, or retinal perfusion and oxygenation. Discordance between these domains may persist despite improvement in blood pressure or cardiac output, supporting serial multimodal rather than single-variable interpretation. However, substantial heterogeneity in acquisition protocols, measurement sites, devices, analytical methods, and proposed thresholds limits comparability and clinical implementation. Conclusion Microcirculatory monitoring should currently be viewed as a complementary framework for identifying persistent or heterogeneous tissue hypoperfusion beyond conventional macrocirculatory targets. Its integration into individualized resuscitation remains promising but requires standardized methodology, external validation, and prospective interventional evidence before any single modality or multimodal strategy can be adopted as a validated resuscitation endpoint.

A ministra da Saúde admitiu hoje que a falta de anestesiologistas constitui um “grande problema” em Lisboa e Vale do Tejo, que poderá ser resolvido com a partilha de recursos entre hospitais, no âmbito das futuras urgências centralizadas.

Background Supraventricular arrhythmias are frequent in critically ill patients and landiolol, an ultra-short-acting, highly β1-selective adrenergic blocker, is increasingly used for their management. Its efficacy and dosing have been described, but its early hemodynamic tolerance at the bedside — when intolerance occurs, how it presents, and which patients are at risk — remains poorly characterized, particularly in vasopressor-dependent patients under-represented in existing cohorts. We aimed to describe the hemodynamic tolerance of landiolol and to identify bedside predictors of poor tolerance. Methods We conducted a retrospective single-center study in patients admitted to the intensive care unit who received landiolol for supraventricular arrhythmia between January 2021 and February 2023. Hemodynamic variables, including pulse pressure, were recorded at baseline (H0) and at H1, H2, H4, H6 and H24. A hemodynamic adverse event was defined as a composite of mean arterial pressure below 64 mmHg, bradycardia below 50 bpm, or a more than 50% increase in vasopressor dose, counted only while landiolol was infused. Predictors of poor tolerance were identified by multivariable logistic regression. Results Among 133 patients (median age 68 years; SAPS II 51; sepsis 54.9%; vasopressors 49.6%), a hemodynamic adverse event occurred in 27 (20.3%), mostly within the first six hours. Events consisted of hypotension or vasopressor escalation; no patient developed bradycardia below 50 bpm. A lower diastolic pressure (adjusted OR 1.05 per 1-mmHg decrease, 95% CI 1.01–1.10) and vasopressor use at initiation (adjusted OR 3.00, 95% CI 1.14–7.91) were independently associated with poor tolerance. Heart rate control was achieved without deterioration of arterial pressure, pulse pressure, ventricular function, or tissue perfusion. Conversion to sinus rhythm was more frequent in new-onset than in pre-existing atrial fibrillation (54.4% vs. 27.9%; p = 0.004). Conclusion In critically ill patients, hemodynamic intolerance to landiolol occurred in one-fifth of cases, arose early, and took the form of hypotension or increased vasopressor requirements rather than bradycardia. A low diastolic pressure and vasopressor dependence identified patients at risk, supporting cautious, individualized use with close monitoring during early titration.

System gives patients, loved ones and health workers the right to ask for a second opinion on care

Background:Ephedrine has been suggested to improve cerebral microcirculation and perfusion compared with phenylephrine. However, prospective...

Background:Ephedrine has been suggested to improve cerebral microcirculation and perfusion compared with phenylephrine. However, prospective...

Background To support hemodynamic management in vasoplegic shock, we previously developed a closed-loop automated infusion system of norepinephrine (NE) and fluid to automatically restore arterial pressure (AP) and cardiac output (CO). To enhance the practical feasibility and efficacy of the system, we integrated a minimally invasive CO monitor and a closed-loop control of vasopressin (AVP) infusion to the system and validated the integrated system in dogs with endotoxin-induced shock. Methods Based on the circulatory equilibrium framework, the system directly controls systemic vascular resistance and stressed blood volume by titrating NE and Ringer’s acetate solution (RiA), respectively, thereby restoring AP and CO. AVP is automatically initiated once infusion rate of NE is increased higher than 1 μg·kg⁻1·min⁻1. The minimally invasive CO monitor estimates CO (COes) by a machine-learning analysis of the peripheral AP contour. In eight anesthetized dogs, the system was implemented, and reference CO (COref) was measured using an aortic flow probe to calibrate COes and track reference hemodynamics. Endotoxin shock was induced via intravenous lipopolysaccharide infusions. After the target AP and COes were set to 70 mmHg and 132 (132–133) mL·min−1·kg−1, respectively, the system was activated. Results The lipopolysaccharide infusion significantly reduced AP from 82 (80–85) to 52 (50–56) mmHg and COref from 132 (125–146) to 90 (80–103) mL·min−1·kg−1, and increased the blood lactate level (LAC) from 21 (21–23) to 36 (32–38) mg·dL−1. Once the system was activated, infusions of NE and RiA were automatically initiated. Infusion of AVP initiated during the system control was associated with significant reduction in NE dose while maintaining AP. Within 5 min after system activation, AP and COes were recovered to >65 mmHg and >122 (122–123) ml·min−1·kg−1, respectively. The median absolute performance errors for AP and COes were <5%. At 60 min after system activation, AP and COref significantly increased to 72 (68–75) mmHg and 130 (127–137) ml·min−1·kg−1 and LAC significantly decreased to 26 (25–28) mg·dL−1 relative to the values observed at endotoxin shock. COes tracked directional changes in COref reasonably well. Conclusions This proof-of-concept study validates the feasibility and physiological performance of the system for the hemodynamic management of vasoplegic shock.

Background To support hemodynamic management in vasoplegic shock, we previously developed a closed-loop automated infusion system of norepinephrine (NE) and fluid to automatically restore arterial pressure (AP) and cardiac output (CO). To enhance the practical feasibility and efficacy of the system, we integrated a minimally invasive CO monitor and a closed-loop control of vasopressin (AVP) infusion to the system and validated the integrated system in dogs with endotoxin-induced shock. Methods Based on the circulatory equilibrium framework, the system directly controls systemic vascular resistance and stressed blood volume by titrating NE and Ringer’s acetate solution (RiA), respectively, thereby restoring AP and CO. AVP is automatically initiated once infusion rate of NE is increased higher than 1 μg·kg⁻1·min⁻1. The minimally invasive CO monitor estimates CO (COes) by a machine-learning analysis of the peripheral AP contour. In eight anesthetized dogs, the system was implemented, and reference CO (COref) was measured using an aortic flow probe to calibrate COes and track reference hemodynamics. Endotoxin shock was induced via intravenous lipopolysaccharide infusions. After the target AP and COes were set to 70 mmHg and 132 (132–133) mL·min−1·kg−1, respectively, the system was activated. Results The lipopolysaccharide infusion significantly reduced AP from 82 (80–85) to 52 (50–56) mmHg and COref from 132 (125–146) to 90 (80–103) mL·min−1·kg−1, and increased the blood lactate level (LAC) from 21 (21–23) to 36 (32–38) mg·dL−1. Once the system was activated, infusions of NE and RiA were automatically initiated. Infusion of AVP initiated during the system control was associated with significant reduction in NE dose while maintaining AP. Within 5 min after system activation, AP and COes were recovered to >65 mmHg and >122 (122–123) ml·min−1·kg−1, respectively. The median absolute performance errors for AP and COes were <5%. At 60 min after system activation, AP and COref significantly increased to 72 (68–75) mmHg and 130 (127–137) ml·min−1·kg−1 and LAC significantly decreased to 26 (25–28) mg·dL−1 relative to the values observed at endotoxin shock. COes tracked directional changes in COref reasonably well. Conclusions This proof-of-concept study validates the feasibility and physiological performance of the system for the hemodynamic management of vasoplegic shock.

Objectives:The role of ketamine for analgosedation in the ICU remains unclear. This study aimed to assess the efficacy of low-dose ketamine infusion...

Objectives:The role of ketamine for analgosedation in the ICU remains unclear. This study aimed to assess the efficacy of low-dose ketamine infusion...

Pending Publication

Pending Publication

Post-cardiac arrest care remains challenging, with persistently poor neurological and survival outcomes. Accordingly, novel adjunctive interventions are needed. While maintaining normocapnia is the current standard, hypercapnia has been proposed as a potential intervention. However, its role and potential benefits remain unclear. This comprehensive review summarizes current evidence on the use of hypercapnia in post-cardiac arrest care, focusing on neurological, cardiovascular, and survival outcomes, underlying mechanisms, and directions for future clinical investigations. Observational studies have sparked interest in the potential benefits of hypercapnia during the post-cardiac arrest period, including in specific populations. Methodological variations and conflicting findings from earlier studies have prompted the conduct of controlled trials and animal experiments to clarify its effects. Mild hypercapnia appears to be a practical and clinically safe approach, improving cerebral oxygenation without major adverse events. However, no improvement in long-term neurological recovery or survival has been demonstrated. Moreover, the effects on the cardiovascular and other organ systems, as well as mechanisms at the cellular level, remain inconclusive. Although mild hypercapnia may be considered part of a comprehensive post-cardiac arrest care strategy, further studies are needed to define its optimal application, potential synergy with other interventions, the populations most likely to benefit, and its underlying mechanisms.

Post-cardiac arrest care remains challenging, with persistently poor neurological and survival outcomes. Accordingly, novel adjunctive interventions are needed. While maintaining normocapnia is the current standard, hypercapnia has been proposed as a potential intervention. However, its role and potential benefits remain unclear. This comprehensive review summarizes current evidence on the use of hypercapnia in post-cardiac arrest care, focusing on neurological, cardiovascular, and survival outcomes, underlying mechanisms, and directions for future clinical investigations. Observational studies have sparked interest in the potential benefits of hypercapnia during the post-cardiac arrest period, including in specific populations. Methodological variations and conflicting findings from earlier studies have prompted the conduct of controlled trials and animal experiments to clarify its effects. Mild hypercapnia appears to be a practical and clinically safe approach, improving cerebral oxygenation without major adverse events. However, no improvement in long-term neurological recovery or survival has been demonstrated. Moreover, the effects on the cardiovascular and other organ systems, as well as mechanisms at the cellular level, remain inconclusive. Although mild hypercapnia may be considered part of a comprehensive post-cardiac arrest care strategy, further studies are needed to define its optimal application, potential synergy with other interventions, the populations most likely to benefit, and its underlying mechanisms.

Проверка показала, что в операционных не были закреплены кислородные баллоны, помещения были тесными, а инструменты для липосакции обрабатывались с нарушением инструкций.

Background Fluid responsiveness assessment guides hemodynamic management in mechanically ventilated critically ill and perioperative patients, but direct cardiac output monitoring is not always available. Under stable ventilation and carbon dioxide production, dynamic EtCO₂ changes may reflect preload-induced changes in pulmonary blood flow and cardiac output. We evaluated the diagnostic accuracy of EtCO₂/PETCO₂ changes for predicting fluid responsiveness during preload challenge in mechanically ventilated adults. Methods PubMed, Embase, Web of Science, the Cochrane Library, and ClinicalTrials.gov were searched from inception to July 12, 2026. Eligible studies evaluated dynamic EtCO₂/PETCO₂ changes during passive leg raising, mini-fluid challenge, or volume expansion in mechanically ventilated adults against an independent cardiac output-, cardiac index-, stroke volume-, stroke volume index-, or LVOT-VTI-based reference standard. Pooled sensitivity and specificity were estimated using a bivariate random-effects model, and reported AUCs were synthesized after logit transformation using a random-effects model. Prespecified subgroup analyses and univariable meta-regression explored clinical and methodological sources of heterogeneity. Risk of bias and certainty of evidence were assessed using QUADAS-2 and GRADE. Results Twenty studies involving mechanically ventilated adults were included, contributing 1,515 diagnostic observations or test conditions. Eighteen studies contributed 2 × 2 data, with pooled sensitivity of 0.748 (95% CI, 0.680–0.806), specificity of 0.853 (95% CI, 0.797–0.895), and SROC AUC of 0.872. Across all 20 studies, the random-effects pooled reported AUC was 0.839 (95% CI, 0.788–0.879). Exploratory subgroup analyses suggested numerically higher estimates for PLR-based assessment, relative thresholds, septic shock cohorts, and patient-level analyses, without establishing subgroup superiority. QUADAS-2 raised frequent concerns about index-test thresholds and reference-standard reporting; GRADE rated the certainty of evidence as low. Conclusions Dynamic EtCO₂/PETCO₂ changes may provide a useful non-invasive adjunct for assessing fluid responsiveness during standardized preload challenge in mechanically ventilated adults under stable ventilatory conditions. They should not be used as a standalone rule-in or rule-out test, and the available evidence does not support a universal threshold.

Background Fluid responsiveness assessment guides hemodynamic management in mechanically ventilated critically ill and perioperative patients, but direct cardiac output monitoring is not always available. Under stable ventilation and carbon dioxide production, dynamic EtCO₂ changes may reflect preload-induced changes in pulmonary blood flow and cardiac output. We evaluated the diagnostic accuracy of EtCO₂/PETCO₂ changes for predicting fluid responsiveness during preload challenge in mechanically ventilated adults. Methods PubMed, Embase, Web of Science, the Cochrane Library, and ClinicalTrials.gov were searched from inception to July 12, 2026. Eligible studies evaluated dynamic EtCO₂/PETCO₂ changes during passive leg raising, mini-fluid challenge, or volume expansion in mechanically ventilated adults against an independent cardiac output-, cardiac index-, stroke volume-, stroke volume index-, or LVOT-VTI-based reference standard. Pooled sensitivity and specificity were estimated using a bivariate random-effects model, and reported AUCs were synthesized after logit transformation using a random-effects model. Prespecified subgroup analyses and univariable meta-regression explored clinical and methodological sources of heterogeneity. Risk of bias and certainty of evidence were assessed using QUADAS-2 and GRADE. Results Twenty studies involving mechanically ventilated adults were included, contributing 1,515 diagnostic observations or test conditions. Eighteen studies contributed 2 × 2 data, with pooled sensitivity of 0.748 (95% CI, 0.680–0.806), specificity of 0.853 (95% CI, 0.797–0.895), and SROC AUC of 0.872. Across all 20 studies, the random-effects pooled reported AUC was 0.839 (95% CI, 0.788–0.879). Exploratory subgroup analyses suggested numerically higher estimates for PLR-based assessment, relative thresholds, septic shock cohorts, and patient-level analyses, without establishing subgroup superiority. QUADAS-2 raised frequent concerns about index-test thresholds and reference-standard reporting; GRADE rated the certainty of evidence as low. Conclusions Dynamic EtCO₂/PETCO₂ changes may provide a useful non-invasive adjunct for assessing fluid responsiveness during standardized preload challenge in mechanically ventilated adults under stable ventilatory conditions. They should not be used as a standalone rule-in or rule-out test, and the available evidence does not support a universal threshold.

Background The perfusion index (PI) is a continuously available pulse oximetry-derived marker of peripheral perfusion; however, its relationship with perioperative metabolic stress remains unclear. Although previous studies have examined intraoperative PI-related metrics and postoperative outcomes, whether the minimum intraoperative PI (PI min) is associated with end-of-surgery hyperlactatemia has not been well characterized. This study aimed to examine the association between PI min and end-of-surgery hyperlactatemia in patients undergoing surgery under general anesthesia. Methods This single-center retrospective observational study reviewed 1,948 consecutive surgical cases performed under general anesthesia. Of these, 186 patients with intraoperative radial arterial catheterization and arterial blood gas analysis performed between the start of wound closure and operating room exit were included in the analysis. PI min was defined as the lowest PI recorded during surgery, excluding cardiopulmonary bypass periods. The primary outcome was end-of-surgery hyperlactatemia, defined as lactate > 2.0 mmol/L. Results Hyperlactatemia occurred in 40 patients (21.5%). Lower PI min was associated with hyperlactatemia (p = 0.019), and this association remained significant after adjustment for age, sex, and surgical category (adjusted odds ratio per 0.1-unit increase, 0.73; 95% confidence interval, 0.57–0.95; p = 0.017). Receiver operating characteristic analysis showed modest discrimination (area under the curve, 0.657), with an exploratory ROC-derived cutoff of PI min < 0.08. PI min was moderately correlated with the time-weighted mean PI. Conclusions Lower PI min was associated with end-of-surgery hyperlactatemia in patients undergoing general anesthesia with intraoperative arterial catheterization. To our knowledge, this study is among the first to specifically link the intraoperative PI nadir with end-of-surgery hyperlactatemia. PI min may serve as a simple intraoperative marker associated with metabolic evidence of hypoperfusion-related stress, although its discriminative performance was modest and prospective validation is required.

Background The perfusion index (PI) is a continuously available pulse oximetry-derived marker of peripheral perfusion; however, its relationship with perioperative metabolic stress remains unclear. Although previous studies have examined intraoperative PI-related metrics and postoperative outcomes, whether the minimum intraoperative PI (PI min) is associated with end-of-surgery hyperlactatemia has not been well characterized. This study aimed to examine the association between PI min and end-of-surgery hyperlactatemia in patients undergoing surgery under general anesthesia. Methods This single-center retrospective observational study reviewed 1,948 consecutive surgical cases performed under general anesthesia. Of these, 186 patients with intraoperative radial arterial catheterization and arterial blood gas analysis performed between the start of wound closure and operating room exit were included in the analysis. PI min was defined as the lowest PI recorded during surgery, excluding cardiopulmonary bypass periods. The primary outcome was end-of-surgery hyperlactatemia, defined as lactate > 2.0 mmol/L. Results Hyperlactatemia occurred in 40 patients (21.5%). Lower PI min was associated with hyperlactatemia (p = 0.019), and this association remained significant after adjustment for age, sex, and surgical category (adjusted odds ratio per 0.1-unit increase, 0.73; 95% confidence interval, 0.57–0.95; p = 0.017). Receiver operating characteristic analysis showed modest discrimination (area under the curve, 0.657), with an exploratory ROC-derived cutoff of PI min < 0.08. PI min was moderately correlated with the time-weighted mean PI. Conclusions Lower PI min was associated with end-of-surgery hyperlactatemia in patients undergoing general anesthesia with intraoperative arterial catheterization. To our knowledge, this study is among the first to specifically link the intraoperative PI nadir with end-of-surgery hyperlactatemia. PI min may serve as a simple intraoperative marker associated with metabolic evidence of hypoperfusion-related stress, although its discriminative performance was modest and prospective validation is required.

Norepinephrine is the first-line vasopressor in septic shock, yet prolonged catecholamine exposure is associated with adverse effects that have prompted growing interest in catecholamine-sparing strategies. This review highlights current evidence on the rationale for catecholamine use, the burden of sustained adrenergic exposure, and current and emerging sparing strategies. Early norepinephrine initiation, including via peripheral access, shortens hypotension duration and reduces fluid requirements. However, catecholamine exposure can carry dose-dependent cardiac, metabolic, and immunological consequences. Perfusion-guided strategies, including individualization of blood pressure targets and titration of vasopressor use based on capillary refill time, represent the cornerstone of reduction of catecholamines. Among alternative non-adrenergic vasopressors, vasopressin reduces catecholamine exposure and the risk of atrial fibrillation, with potential renal benefits. Angiotensin II represents an option in catecholamine-refractory shock, with post-hoc evidence suggesting benefit in patients with acute kidney injury or elevated renin concentrations. Inhibition of circulating dipeptidyl peptidase 3, which degrades angiotensin II, is an emerging therapeutic strategy. Corticosteroids restore vasopressor sensitivity and accelerate catecholamine weaning. Short-acting β1-blockers have shown hemodynamic promise but inconsistent outcomes, underscoring the need for better patient selection. Methylene blue, targeting the vasodilatory nitric oxide pathway, represents another strategy. Finally, emerging immunomodulatory approaches, including extracellular histone neutralization and polymyxin B hemoperfusion in endotoxin phenotypes, aim to attenuate the dysregulated host response driving vasopressor dependency. A personalized and multimodal approach, including perfusion-guided targets, non-adrenergic vasopressors, and phenotype-based patient selection, represents the most promising strategy to reduce potential consequences of adrenergic burden while maintaining tissue perfusion.

Norepinephrine is the first-line vasopressor in septic shock, yet prolonged catecholamine exposure is associated with adverse effects that have prompted growing interest in catecholamine-sparing strategies. This review highlights current evidence on the rationale for catecholamine use, the burden of sustained adrenergic exposure, and current and emerging sparing strategies. Early norepinephrine initiation, including via peripheral access, shortens hypotension duration and reduces fluid requirements. However, catecholamine exposure can carry dose-dependent cardiac, metabolic, and immunological consequences. Perfusion-guided strategies, including individualization of blood pressure targets and titration of vasopressor use based on capillary refill time, represent the cornerstone of reduction of catecholamines. Among alternative non-adrenergic vasopressors, vasopressin reduces catecholamine exposure and the risk of atrial fibrillation, with potential renal benefits. Angiotensin II represents an option in catecholamine-refractory shock, with post-hoc evidence suggesting benefit in patients with acute kidney injury or elevated renin concentrations. Inhibition of circulating dipeptidyl peptidase 3, which degrades angiotensin II, is an emerging therapeutic strategy. Corticosteroids restore vasopressor sensitivity and accelerate catecholamine weaning. Short-acting β1-blockers have shown hemodynamic promise but inconsistent outcomes, underscoring the need for better patient selection. Methylene blue, targeting the vasodilatory nitric oxide pathway, represents another strategy. Finally, emerging immunomodulatory approaches, including extracellular histone neutralization and polymyxin B hemoperfusion in endotoxin phenotypes, aim to attenuate the dysregulated host response driving vasopressor dependency. A personalized and multimodal approach, including perfusion-guided targets, non-adrenergic vasopressors, and phenotype-based patient selection, represents the most promising strategy to reduce potential consequences of adrenergic burden while maintaining tissue perfusion.

MOH, national trauma, network, patients, care, Ma

Background Over 50% of patients receiving veno-arterial extracorporeal membrane oxygenation (VA-ECMO) die, mostly due to inadequate cardiac recovery. Moderate-to-high positive end-expiratory pressure (PEEP) may positively influence cardiac recovery and survival by optimizing biventricular loading conditions through improved heart-lung interaction. Methods Participants in the multicenter observational cohort study (PRECISE-ECLS) were eligible if they received VA-ECMO support for more than 24 h in one of the six participating Dutch ICUs (2016–2024) and had longitudinal PEEP data for the first 48 h. Hemodynamic and respiratory parameters were assessed over 5 days, stratified by PEEP group. Associations between cumulative PEEP exposure and outcomes, including 30-day VA-ECMO weaning failure as primary endpoint and mortality, were assessed using time-dependent joint models integrating longitudinal PEEP trajectories with time-to-event analyses. Results 409 VA-ECMO-supported patients (mean age 59 years, 70% male) were categorized into a low (≤ 8 cmH₂O; n = 191), intermediate (8.1–13.9 cmH₂O; n = 169), and high (≥ 14 cmH₂O; n = 49) PEEP group. PEEP levels were comparable before versus after VA-ECMO initiation (median difference 0 cmH₂O; IQR − 1 to 2). Compared with low PEEP, higher PEEP levels were applied to sicker patients and were not accompanied by clear adverse temporal trends in the hemodynamic or respiratory variables examined. Higher cumulative PEEP exposure was not significantly associated with the hazard of 30-day VA-ECMO weaning failure (HR 0.97, 95% CI 0.92–1.01) and mortality (HR 0.96, 95% CI 0.90–1.02). Conclusions PEEP levels remained largely unchanged after VA-ECMO initiation. Higher PEEP was preferentially applied to patients with greater illness severity, and no consistent adverse temporal trends were observed in the measured hemodynamic or respiratory variables. Among patients surviving beyond the first 24 h, cumulative PEEP exposure was not significantly associated with 30-day risks of VA-ECMO weaning failure and mortality. Trial registration ClinicalTrials.gov; NCT05444764; first posted on July 6th, 2022.

Background Over 50% of patients receiving veno-arterial extracorporeal membrane oxygenation (VA-ECMO) die, mostly due to inadequate cardiac recovery. Moderate-to-high positive end-expiratory pressure (PEEP) may positively influence cardiac recovery and survival by optimizing biventricular loading conditions through improved heart-lung interaction. Methods Participants in the multicenter observational cohort study (PRECISE-ECLS) were eligible if they received VA-ECMO support for more than 24 h in one of the six participating Dutch ICUs (2016–2024) and had longitudinal PEEP data for the first 48 h. Hemodynamic and respiratory parameters were assessed over 5 days, stratified by PEEP group. Associations between cumulative PEEP exposure and outcomes, including 30-day VA-ECMO weaning failure as primary endpoint and mortality, were assessed using time-dependent joint models integrating longitudinal PEEP trajectories with time-to-event analyses. Results 409 VA-ECMO-supported patients (mean age 59 years, 70% male) were categorized into a low (≤ 8 cmH₂O; n = 191), intermediate (8.1–13.9 cmH₂O; n = 169), and high (≥ 14 cmH₂O; n = 49) PEEP group. PEEP levels were comparable before versus after VA-ECMO initiation (median difference 0 cmH₂O; IQR − 1 to 2). Compared with low PEEP, higher PEEP levels were applied to sicker patients and were not accompanied by clear adverse temporal trends in the hemodynamic or respiratory variables examined. Higher cumulative PEEP exposure was not significantly associated with the hazard of 30-day VA-ECMO weaning failure (HR 0.97, 95% CI 0.92–1.01) and mortality (HR 0.96, 95% CI 0.90–1.02). Conclusions PEEP levels remained largely unchanged after VA-ECMO initiation. Higher PEEP was preferentially applied to patients with greater illness severity, and no consistent adverse temporal trends were observed in the measured hemodynamic or respiratory variables. Among patients surviving beyond the first 24 h, cumulative PEEP exposure was not significantly associated with 30-day risks of VA-ECMO weaning failure and mortality. Trial registration ClinicalTrials.gov; NCT05444764; first posted on July 6th, 2022.

Purpose To evaluate outcomes of a multimodal prehabilitation service for cancer surgery patients delivered through three pathways (Specialised, Targeted, Universal) within routine NHS care at Nottingham University Hospitals NHS Trust. Methods This was a retrospective observational service evaluation of routine care data collected between 2022 and 2025. Of 1961 referred patients, 1720 were analysed: Specialised (n = 329), Targeted (n = 943), and Universal (n = 448). Multimodal prehabilitation included exercise, nutrition, and psychological support, stratified by risk. Functional capacity was assessed using the Incremental Shuttle Walk Test (ISWT), 60-s Sit-to-Stand (STS), and grip strength. Psychological well-being was measured using the Generalised Anxiety Disorder-7 (GAD-7), and Patient Health Questionnaire-9 (PHQ-9). Physical activity behaviour was also recorded. Results All pathways showed significant within-group improvements. ISWT increased by 57 m (p < 0.001, d = 0.6) and STS by 6 repetitions (p < 0.001, d = 0.9). Anxiety (Δ –1.9) and depression (Δ –2.0) scores decreased (both p < 0.001, d ≈ –0.5). Weekly physical activity rose by 142 min (d = 1.07), and strength sessions increased by 2.4 per week (d = 1.1). Between-group differences were limited: PHQ-9 improved more in Specialised versus Targeted, and strength sessions increased more in Universal versus Targeted. Conclusion A tiered, multimodal prehabilitation service integrated into cancer pathways produced meaningful functional, psychological, and behavioural benefits, supporting broader implementation and improved patient access.

Purpose To evaluate outcomes of a multimodal prehabilitation service for cancer surgery patients delivered through three pathways (Specialised, Targeted, Universal) within routine NHS care at Nottingham University Hospitals NHS Trust. Methods This was a retrospective observational service evaluation of routine care data collected between 2022 and 2025. Of 1961 referred patients, 1720 were analysed: Specialised (n = 329), Targeted (n = 943), and Universal (n = 448). Multimodal prehabilitation included exercise, nutrition, and psychological support, stratified by risk. Functional capacity was assessed using the Incremental Shuttle Walk Test (ISWT), 60-s Sit-to-Stand (STS), and grip strength. Psychological well-being was measured using the Generalised Anxiety Disorder-7 (GAD-7), and Patient Health Questionnaire-9 (PHQ-9). Physical activity behaviour was also recorded. Results All pathways showed significant within-group improvements. ISWT increased by 57 m (p < 0.001, d = 0.6) and STS by 6 repetitions (p < 0.001, d = 0.9). Anxiety (Δ –1.9) and depression (Δ –2.0) scores decreased (both p < 0.001, d ≈ –0.5). Weekly physical activity rose by 142 min (d = 1.07), and strength sessions increased by 2.4 per week (d = 1.1). Between-group differences were limited: PHQ-9 improved more in Specialised versus Targeted, and strength sessions increased more in Universal versus Targeted. Conclusion A tiered, multimodal prehabilitation service integrated into cancer pathways produced meaningful functional, psychological, and behavioural benefits, supporting broader implementation and improved patient access.

Background Current recommendations for intraoperative blood pressure management suggest maintaining mean arterial pressure (MAP) at ≥ 60–65 mmHg to avoid hypotension. However, controversy remains regarding whether higher or individualized MAP targets improve clinically important outcomes in surgical patients. We aimed to determine whether intensive intraoperative blood pressure management, defined as higher fixed or individualized MAP targets, reduces major postoperative morbidity compared with standard management (MAP ≥ 60–65 mmHg). Methods We systematically searched PubMed, Embase, the Cochrane Library, and Web of Science for randomized controlled trials (RCTs) comparing intensive and standard intraoperative blood pressure management in adults undergoing noncardiac surgery. The primary outcomes were postoperative myocardial injury, postoperative delirium (POD), and acute kidney injury (AKI). Secondary outcomes included postoperative mortality, stroke, heart failure, acute respiratory distress syndrome (ARDS), pneumonia, intensive care unit (ICU) admission, surgical site infection (SSI), and hospital length of stay (LOS). Data were pooled using a random-effects model with the Hartung–Knapp adjustment. Risk ratios (RR) were calculated for dichotomous outcomes, and mean differences (MD) were calculated for continuous outcomes. Trial sequential analysis (TSA) was performed to control for random error and assess the conclusiveness of the available evidence. Results Eighteen RCTs involving 16,573 patients were included. Compared with standard management, intensive management was associated with lower risks of POD (10 studies; RR = 0.72, 95% CI [0.55, 0.93]; P = 0.019; moderate-certainty evidence) and SSI (5 studies; RR = 0.64, 95% CI [0.53, 0.76]; P = 0.002; moderate-certainty evidence). However, no significant between-group differences were observed in postoperative myocardial injury (9 studies; RR = 1.02, 95% CI [0.92, 1.13]), AKI (13 studies; RR = 0.92, 95% CI [0.79, 1.06]), or mortality (13 studies; RR = 0.99, 95% CI [0.83, 1.17]). TSA supported a beneficial effect of intensive management on POD, and indicated that a clinically meaningful benefit of the prespecified magnitude was unlikely for myocardial injury and AKI. No significant between-group differences were observed in postoperative stroke, pneumonia, heart failure, ICU admission, or hospital LOS. Conclusions In this systematic review and meta-analysis, intensive intraoperative blood pressure management may reduce the risks of POD and SSI in adults undergoing noncardiac surgery. However, it was not associated with significant differences in postoperative myocardial injury, AKI or mortality. Protocol registration PROSPERO: CRD420261323873.