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Background: Reusing anaesthesia infusion-set components may reduce the climate impact from plastic waste and discarded medications. Infusion-set contents can be shielded from patient contact by single use of an infusion line fitted with dual antireflux valves, preventing retrograde entry of microorganisms, and eliminating the risk for patient-to-patient cross-contamination. However, infusion-set contamination from compromised aseptic handling could affect quality of care., Interventions: To determine the prevalence of infusion-set bacterial contamination and compare the climate effects, we randomised operating rooms scheduled for total intravenous anaesthesia to handle procedures by infusion-set reuse or single-use. Both methods used dual single-use antireflux valves., Outcomes: The primary outcome was infusion-set bacterial contamination assessed by aerobic culture of infusion-set fluid collected after each procedure. The secondary outcome was CO 2 emissions (CO 2 -eq) estimated by life cycle assessment of component and medication use. To assess feasibility of detecting an inter-method difference in bacterial contamination, an interim analysis was planned after including at least 150 procedures per group., Results: After allocating 54 operating rooms per method, 189 and 159 procedures of reuse and single use were included. Reuse permitted a median of three procedures per infusion set (range 1 to 8). Positive cultures occurred in two procedures per method [mean (95% CI)]; prevalence 1.15% (0.03 to 2.27); relative risk of reuse versus single use 0.84 (0.12 to 5.93), P  = 0.861. As prespecified, inclusion was stopped due to futility. The median (95% CI) per-procedure climate emissions were 0.43 (0.41 to 0.47) and 1.39 (1.37 to 1.40) kg CO 2 -eq for reuse and single-use respectively; difference -0.96 (-0.99 to -0.93), P  < 0.0005. The main sources for climate emissions were production of infusion-set components and waste handling., Conclusions: We conclude that the prevalence of bacterial contamination was low for both methods. A much larger study would be needed to detect an inter-method difference. Reuse of infusion-set components allowed significantly reduced intravenous anaesthesia climate emissions., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the European Society of Anaesthesiology.)

Background: To optimize right ventricular-pulmonary coupling during veno-arterial (VA) ECMO weaning, inotropes, vasopressors and/or vasodilators are used to change right ventricular (RV) function (contractility) and pulmonary artery (PA) elastance (afterload). RV-PA coupling is the ratio between right ventricular contractility and pulmonary vascular elastance and as such, is a measure of optimized crosstalk between ventricle and vasculature. Little is known about the physiology of RV-PA coupling during VA ECMO. This study describes adaptive mechanisms for maintaining RV-PA coupling resulting from changing pre- and afterload conditions in VA ECMO., Methods: In 13 pigs, extracorporeal flow was reduced from 4 to 1 L/min at baseline and increased afterload (pulmonary embolism and hypoxic vasoconstriction). Pressure and flow signals estimated right ventricular end-systolic elastance and pulmonary arterial elastance. Linear mixed-effect models estimated the association between conditions and elastance., Results: At no extracorporeal flow, end-systolic elastance increased from 0.83 [0.66 to 1.00] mmHg/mL at baseline by 0.44 [0.29 to 0.59] mmHg/mL with pulmonary embolism and by 1.36 [1.21 to 1.51] mmHg/mL with hypoxic pulmonary vasoconstriction (p < 0.001). Pulmonary arterial elastance increased from 0.39 [0.30 to 0.49] mmHg/mL at baseline by 0.36 [0.27 to 0.44] mmHg/mL with pulmonary embolism and by 0.75 [0.67 to 0.84] mmHg/mL with hypoxic pulmonary vasoconstriction (p < 0.001). Coupling remained unchanged (2.1 [1.8 to 2.3] mmHg/mL at baseline; - 0.1 [- 0.3 to 0.1] mmHg/mL increase with pulmonary embolism; - 0.2 [- 0.4 to 0.0] mmHg/mL with hypoxic pulmonary vasoconstriction, p > 0.05). Extracorporeal flow did not change coupling (0.0 [- 0.0 to 0.1] per change of 1 L/min, p > 0.05). End-diastolic volume increased with decreasing extracorporeal flow (7.2 [6.6 to 7.8] ml change per 1 L/min, p < 0.001)., Conclusions: The right ventricle dilates with increased preload and increases its contractility in response to afterload changes to maintain ventricular-arterial coupling during VA extracorporeal membrane oxygenation., (© 2024. The Author(s).)

This review describes the intricate physiological interactions involved in the application of extracorporeal therapy, with specific focus on cardiopulmonary relationships. Extracorporeal therapy significantly influences cardiovascular and pulmonary physiology, highlighting the necessity for clinicians to understand these interactions for improved patient care. Veno-arterial extracorporeal membrane oxygenation (veno-arterial ECMO) unloads the right ventricle and increases left ventricular (LV) afterload, potentially exacerbating LV failure and pulmonary edema. Veno-venous (VV) ECMO presents different challenges, where optimal device and ventilator settings remain unknown. Influences on right heart function and native gas exchange as well as end-expiratory lung volumes are important concepts that should be incorporated into daily practice. Future studies should not be limited to large clinical trials focused on mortality but rather address physiological questions to advance the understanding of extracorporeal therapies. This includes exploring optimal device and ventilator settings in VV ECMO, standardizing cardiopulmonary function monitoring strategies, and developing better strategies for device management throughout their use. In this regard, small human or animal studies and computational physiological modeling may contribute valuable insights into optimizing the management of extracorporeal therapies., Competing Interests: The Department of Intensive Care Medicine, Inselspital Bern has, or has had in the past, research contracts with Abionic SA, AVA AG, CSEM SA, Cube Dx GmbH, Cyto Sorbents Europe GmbH, Edwards Lifesciences LLC, GE Healthcare, ImaCor Inc., MedImmune LLC, Orion Corporation, and Phagenesis Ltd. and research and development/consulting contracts with Edwards Lifesciences LLC, Nestec SA, and Wyss Zurich. The money was paid into a departmental fund; no author received any personal financial gain. The Department of Intensive Care Medicine received unrestricted educational grants from the following organizations for organizing a quarterly postgraduate educational symposium, the Berner Forum for Intensive Care (until 2015): Abbott AG, Anandic Medical Systems, Astellas, AstraZeneca, Bard Medica SA, Baxter, B &verbar; Braun, CSL Behring, Covidien, Fresenius Kabi, GSK, Lilly, Maquet, MSD, Novartis, Nycomed, Orion Pharma, Pfizer, and Pierre Fabre Pharma AG (formerly known as RobaPharm). The Department of Intensive Care Medicine has received unrestricted educational grants from the following organizations for organizing biannual postgraduate courses in the fields of critical care ultrasound, management of extracorporeal membrane oxygenation, and mechanical ventilation: Abbott AG, Anandic Medical Systems, Bard Medica SA., Bracco, Dräger Schweiz AG, Edwards Lifesciences AG, Fresenius Kabi (Schweiz) AG, Getinge Group Maquet AG, Hamilton Medical AG, Pierre Fabre Pharma AG (formerly known as RobaPharm), PanGas AG Healthcare, Pfizer AG, Orion Pharma, and Teleflex Medical GmbH., (Copyright © 2023 Bachmann, Berger and Moller.)

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Collapsibility of caval vessels and stroke volume and pulse pressure variations (SVV, PPV) are used as indicators of volume responsiveness. Their behavior under increasing airway pressures and changing right ventricular afterload is incompletely understood. If the phenomena of SVV and PPV augmentation are manifestations of decreasing preload, they should be accompanied by decreasing transmural right atrial pressures. Eight healthy pigs equipped with ultrasonic flow probes on the pulmonary artery were exposed to positive end-expiratory pressure of 5 and 10 cmH 2 O and three volume states ( Euvolemia , defined as SVV < 10%, Bleeding , and Retransfusion ). SVV and PPV were calculated for the right and PPV for the left side of the circulation at increasing inspiratory airway pressures (15, 20, and 25 cmH 2 O). Right ventricular afterload was assessed by surrogate flow profile parameters. Transmural pressures in the right atrium and the inferior and superior caval vessels (IVC and SVC) were determined. Increasing airway pressure led to increases in ultrasonic surrogate parameters of right ventricular afterload, increasing transmural pressures in the right atrium and SVC, and a drop in transmural IVC pressure. SVV and PPV increased with increasing airway pressure, despite the increase in right atrial transmural pressure. Right ventricular stroke volume variation correlated with indicators of right ventricular afterload. This behavior was observed in both PEEP levels and all volume states. Stroke volume variation may reflect changes in right ventricular afterload rather than changes in preload. NEW & NOTEWORTHY Stroke volume variation and pulse pressure variation are used as indicators of preload or volume responsiveness of the heart. Our study shows that these variations are influenced by changes in right ventricular afterload and may therefore reflect right ventricular failure rather than pure volume responsiveness. A zone of collapse detaches the superior vena cava and its diameter variation from the right atrium.

High portal venous blood flow (Qpv) may contribute to posthepatectomy liver failure. Both Trendelenburg position (TP) and elevated airway pressure (Paw) increase backpressure to venous return and may thereby reduce Qpv. The aim of this study was to evaluate the effects of TP and increased Paw on hepatosplanchnic hemodynamics before and after major liver resection. Arterial and venous blood pressures, Qpv, extrasplanchnic inferior vena cava (Qivc), superior mesenteric (Qsma), hepatic (Qha), and carotid artery blood flows (Qca) were measured in 14 anesthetized and mechanically ventilated pigs in supine and 30° TP during end-expiratory hold at 5 cmH 2 O positive end-expiratory pressure (PEEP) and during inspiratory hold with Paw of 15, 20, 25, and 30 cmH 2 O. After major liver resection, the interventions were repeated in seven randomly selected animals. At baseline, TP increased right atrial pressure (Pra) and Qpv but not Qivc or Qsma. With increased Paw in the supine position, Pra increased and all regional blood flows decreased. TP during increasing Paw attenuated the decrease in Qpv, Qsma, and Qivc but not in Qha or Qca. After liver resection, the effects of TP during increasing Paw remained, albeit at higher portal vein pressures. However, TP alone did not increase IVC venous return. Increasing Paw in supine position reduces Qpv and all other regional flows, while the reduction in Qpv is attenuated in TP, suggesting partly preserved liver waterfall or decreased intrahepatic resistance. Liver resection, despite resulting in major intrahepatic blood flow changes, does not fundamentally influence the interaction of increasing Paw and TP on regional perfusion. NEW & NOTEWORTHY In Trendelenburg position (TP), liver blood flow is the only contributor to increased venous return measured in the inferior vena cava (IVC), which attenuates the decreased IVC venous return induced by increasing airway pressure. After liver resection, TP similarly attenuated effects of increasing airway pressure.

Extended liver resection results in loss of a large fraction of the hepatic vascular bed, thereby causing abrupt alterations in perfusion of the remnant liver. Mechanisms of hemodynamic adaptation and associated changes in oxygen metabolism after liver resection and the effect of mechanical portal blood flow reduction were assessed. A pig model ( n = 16) of extended partial hepatectomy was established that included continuous observation for 24 h under general anesthesia. Pigs were randomly separated into two groups, one with a portal flow reduction of 70% compared with preoperative values, and the other as a control ( n = 8, each). In controls, portal flow [mean (SD)] increased from 74 (8) mL·min -1 ·100 g -1 preoperatively to 240 (48) mL·min -1 ·100 g -1 at 6 h after resection ( P < 0.001). Hepatic arterial buffer response was abolished after resection. Oxygen uptake per unit liver mass increased from 4.0 (1.1) mL·min -1 ·100 g -1 preoperatively to 7.7 (1.7) mL·min -1 ·100 g -1 8 h after resection ( P = 0.004). Despite this increase in relative oxygen uptake, total hepatic oxygen consumption (V̇o 2 ) was not maintained, and markers of hypoxia and anaerobic metabolism were significantly increased in hepatocytes after resection. Reduced postoperative portal flow was associated with significantly decreased levels of aspartate aminotransferase and bilirubin and increased hepatic clearance of indocyanine green. In conclusion, major liver resection was associated with persistent portal hyperperfusion, loss of the hepatic arterial buffer response, decreased total hepatic V̇o 2 and with increased anaerobic metabolism. Portal flow modulation by partial portal vein occlusion attenuated liver injury after extended liver resection. NEW & NOTEWORTHY Because of continuous monitoring, the experiments allow precise observation of the influence of liver resection on systemic and local abdominal hemodynamic alterations and oxygen metabolism. Major liver resection is associated with significant and persistent portal hyperperfusion and loss of hepatic arterial buffer response. The correlation of portal hyperperfusion and parameters of liver injury and dysfunction offers a novel therapeutic option to attenuate liver injury after extended liver resection.

Background: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is gaining widespread use in the treatment of severe cardiorespiratory failure. Blood volume expansion is commonly used to increase ECMO flow (QECMO), with risk of positive fluid balance and worsening prognosis. We studied the effects of vasoconstriction on recruitment of blood volume as an alternative for increasing QECMO, based on the concepts of venous return., Methods: In a closed chest, centrally cannulated porcine preparation (n = 9) in ventricular fibrillation and VA-ECMO with vented left atrium, mean systemic filling pressure (MSFP), and venous return driving pressure (VRdP) were determined in Euvolemia, during Vasoconstriction (norepinephrine 0.05, 0.125, and 0.2 μg/kg/min) and after Volume Expansion (3 boluses of 10 mL/kg Ringer's lactate). Maximum achievable QECMO was examined., Results: Vasoconstriction and Volume Expansion both increased maximum achievable QECMO, delivery of oxygen (DO2), and MSFP, but right atrial pressure increased in parallel. VRdP did not change. The vascular elastance curve was shifted to the left by Vasoconstriction, with recruitment of stressed volume. It was shifted to the right by Volume Expansion with direct expansion of stressed volume. Volume Expansion decreased resistance to venous return and pump afterload., Conclusions: In a circulation completely dependent on ECMO support, maximum achievable flow directly depended on the vascular factors governing venous return-i.e., closing conditions, stressed vascular volume and the elastance and resistive properties of the vasculature. Both treatments increased maximum achievable ECMO flow at stable DO2, via increases in stressed volume by different mechanisms. Vascular resistance and pump afterload decreased with Volume Expansion.

Competing Interests: Conflicts of Interest: The authors have no conflicts of interest to declare.

The relevance of right atrial pressure (RAP) as the backpressure for venous return (Q VR ) and mean systemic filling pressure as upstream pressure is controversial during dynamic changes of circulation. To examine the immediate response of Q VR (sum of caval vein flows) to changes in RAP and pump function, we used a closed-chest, central cannulation, heart bypass porcine preparation ( n = 10) with venoarterial extracorporeal membrane oxygenation. Mean systemic filling pressure was determined by clamping extracorporeal membrane oxygenation tubing with open or closed arteriovenous shunt at euvolemia, volume expansion (9.75 ml/kg hydroxyethyl starch), and hypovolemia (bleeding 19.5 ml/kg after volume expansion). The responses of RAP and Q VR were studied using variable pump speed at constant airway pressure (P AW ) and constant pump speed at variable P AW Within each volume state, the immediate changes in Q VR and RAP could be described with a single linear regression, regardless of whether RAP was altered by pump speed or P AW ( r 2 = 0.586-0.984). RAP was inversely proportional to pump speed from zero to maximum flow ( r 2 = 0.859-0.999). Changing P AW caused immediate, transient, directionally opposite changes in RAP and Q VR (RAP: P ≤ 0.002 and Q VR : P ≤ 0.001), where the initial response was proportional to the change in Q VR driving pressure. Changes in P AW generated volume shifts into and out of the right atrium, but their effect on upstream pressure was negligible. Our findings support the concept that RAP acts as backpressure to Q VR and that Guyton's model of circulatory equilibrium qualitatively predicts the dynamic response from changing RAP. NEW & NOTEWORTHY Venous return responds immediately to changes in right atrial pressure. Concomitant volume shifts within the systemic circulation due to an imbalance between cardiac output and venous return have negligible effects on mean systemic filling pressure. Guyton's model of circulatory equilibrium can qualitatively predict the resulting changes in dynamic conditions with right atrial pressure as backpressure to venous return., (Copyright © 2017 the American Physiological Society.)

According to Guyton's model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to venous return (RVR) determine venous return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the effect of positive end-expiratory pressure (PEEP) and blood volume on venous return and MSFP in pigs. MSFP was measured by balloon occlusion of the right atrium (MSFPRAO), and the MSFP obtained via extrapolation of pressure-flow relationships with airway occlusion (MSFPinsp&#95;hold) was extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding, and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, 12.9 (SD 2.5) mmHg; PEEP 10, 14.0 (SD 2.6) mmHg, P = 0.002] without change in QPA [2.75 (SD 0.43) vs. 2.56 (SD 0.45) l/min, P = 0.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (SD 2.2) and 16.4 (SD 3.0) mmHg, respectively, P < 0.001], with parallel changes in QPA Neither PEEP nor volume state altered RVR (P = 0.489). MSFPinsp&#95;hold overestimated MSFPRAO [16.5 (SD 5.8) vs. 13.6 (SD 3.2) mmHg, P = 0.001; mean difference 3.0 (SD 5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightward in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36% (SD 24%) of preinspiratory hold at 15 cmH2O inspiratory pressure], and the QIVC recovery was most complete at the lowest inspiratory pressures independent of volume state [range from 80% (SD 7%) after bleeding to 103% (SD 8%) at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends venous return, possibly via hepatosplanchnic vascular waterfall., (Copyright © 2016 the American Physiological Society.)

Objective: To assess the risk of perforation or hemorrhage of peptic ulcer on treatment with nonsteroidal antiinflammatory drugs (NSAIDs), both as a class and as individual agents., Methods: A case-control study of medication histories in 494 patients and 972 matched control subjects., Results: The increase in risk (odds ratio) with NSAID therapy was 5.1 times the risk in controls. The odds ratio for piroxicam was 6.3 (95% confidence interval [CI] 3.3-12.0), as compared with 2.9 for diclofenac, ketoprofen, and sulindac combined (95% CI 2.0-4.2). The effect of other risk factors was also considered, and the adjusted odds ratios were 4.1 for all NSAIDs, 6.4 (95% CI 2.8-15.0) for piroxicam, and 3.3 (95% CI 2.0-5.5) for diclofenac, ketoprofen, and sulindac combined., Conclusion: The estimate of overall risk of peptic ulcer complications with NSAIDs is similar to that found in other studies. There appear to be differences in risk between agents.

The management of a patient with a large symptomatic rheumatoid pleural effusion is described. Thoracentesis and bed rest gave only short term modest benefit. A more lasting and beneficial response was obtained with an intrapleural injection of (120 mg) depomethylprednisolone acetate. This treatment is a useful interim measure until disease suppressive therapy gives systemic control.

Two cases of mianserin induced neutropenia associated with prolonged elimination of the drug were studied. In each case the pharmacokinetic profile suggested saturable elimination kinetics, and the temporal relation of mianserin concentrations and the neutrophil count suggested a direct toxic effect of mianserin on the bone marrow. Until further studies are carried out the plasma mianserin concentration and neutrophil count should be measured in any patient who develops an infection while taking this drug.

At the onset of Still's disease (systemic-onset juvenile arthritis) in a 12-year-old girl, serological evidence of Coxsackie B virus infection was found. Two weeks later she developed a haemophagocytic syndrome which was then treated with cytotoxic therapy. Her arthritis is still active six years later.

A 29 year old woman with polymyositis treated with azathioprine presented with pneumonia. Rising serum antibody titres have confirmed a diagnosis of legionnaires' disease. Infection with Legionella pneumophila must now be considered in New Zealand when patients present with pneumonia and severe pyrexia, especially if they show known risk factors.