ESICM LIVES Physiology 2026

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Introduction: Intravenous bicarbonate is a commonly used agent in the management of acute metabolic acidosis. However, it’s clinical benefit and safety is largely uncertain. We summarized the existing randomized controlled data and examined whether the use of intravenous bicarbonate, as compared to control or an alternate type of fluid without bicarbonate, leads to improvements in patient-important outcomes in those hospitalized with acute metabolic acidosis. Methods: We searched Ovid MEDLINE, Embase, the Cochrane library, and Clinicaltrials.gov, from inception until Jan 2nd 2026 and included randomized controlled trials of hospitalized adult participants who received intravenous bicarbonate, as compared to control or an alternate type of fluid without bicarbonate, for metabolic acidosis. We excluded studies examining oral bicarbonate. We pooled data using a random-effects model and present risk ratios (RRs) or mean differences (MDs), along with 95% confidence intervals (CIs). We assessed individual study risk of bias using the modified Cochrane tool, and certainty of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Results: Of 1066 citations, we included 9 RCTs (n = 1331 patients), three of which focused on patients exclusively with severe diabetic ketoacidosis, with initial pH values ranging from 7.00 -7.06. Pooled analysis showed that bicarbonate may be associated with decreased mortality (RR 0.93, 95% CI: 0.82–1.05, low certainty), and decreased need for renal replacement therapy (RR 0.69, 95% CI 0.60 to 0.80, low certainty) compared to not using bicarbonate. Bicarbonate may have no effect on length of hospital stay (MD of 0.41 days longer, 95% CI 3.54 fewer to 4.36 days longer, low certainty). Conclusion: Bicarbonate may reduce mortality and need for renal replacement therapy in hospitalized patients with metabolic acidosis, but further data is needed to increase precision in effect estimates and further assess the impact of bicarbonate on other patient-important outcomes.

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Introduction: Severe aortic stenosis (AS) is a recognized risk factor for sudden cardiac death (SCD). While ventricular tachyarrhythmias are the most common immediate cause of SCD, the majority of cases of SCD in patients with severe AS exhibited bradyarrhythmia as the primary rhythm. Enhanced activation of left ventricular baroreceptors (Bezold-Jarisch reflex) has been implicated in the pathogenesis of syncope in patients with AS. However, the precise mechanism by which an otherwise benign circulatory syncope can progress to cardiac arrest in severe AS remains unclear. We propose a hemodynamic-energetic mechanism to explain this progression and demonstrate its plausibility using a mathematical model of cardiac hemodynamics and energetics. Methods: The mathematical model of cardiac hemodynamics and energetics developed in this work is based on the two-element Windkessel model of arterial hemodynamics, the ventriculoarterial coupling model, and ventricular energetics model. The model quantifies energy delivered to the heart by the coronary circulation and energy expenditure of the heart. Under physiological conditions, energy delivery is higher than energy expenditure. Using the model, we examined whether and under which circumstances the opposite situation can arise where energy expenditure is higher than energy delivery. Such a situation does not allow more than very short-term cardiac function and leads inevitably to cardiac arrest. To analyze the model, the influence of individual independent model variables on energies, pressures and stroke volume was assessed, and global sensitivity analysis was performed using Sobol indices. Simulations of syncopal episodes were performed for individuals with a normal aortic valve and with severe AS. Four scenarios were assessed: resting state, isolated pronounced reduction in total peripheral resistance (TPR), TPR reduction with compensatory response, and TPR reduction with concomitant bradycardia. The model was validated against published clinical data to ensure physiological plausibility and consistency. Results: The model identifies states of cardiac energetic imbalance, wherein the energy expenditure of the heart exceeds the energy delivered to it. Analysis of individual independent variable influence indicates that an energy imbalance in AS is precipitated by low aortic valve area (Sao), low TPR, high left ventricular end-diastolic volume (EDV), high end-systolic elastance, high heart rate (HR), low arterial compliance and high coronary vascular resistance (Rcor). Global sensitivity analysis shows that in normal aortic valve or non-severe AS, energy balance is primarily determined by Rcor, TPR and HR, with Rcor being dominant. In severe AS with preserved coronary vasodilatory reserve, Rcor remains most influential, while TPR, Sao and EDV also contribute significantly. When coronary vasodilation is impaired in severe AS, Rcor loses relevance, and energy balance depends mainly on Sao, EDV, and TPR. Other variables have minimal impact. The results of simulation of syncopal episode reveal that in an individual with a normal aortic valve, an isolated profound reduction in TPR results in energy destabilization. However, the compensatory response as well as the concomitant bradycardia serve to reverse this imbalance. In contrast, only the resting situation is energetically stable in case of AS. As in the normal case, an isolated profound reduction in TPR results in energy destabilization. However, neither compensatory response nor concomitant bradycardia can reverse the imbalance. Conclusions: This study proposes a hemodynamic-energetic mechanism to explain how otherwise benign circulatory syncope can progress to cardiac arrest in patients with severe AS and demonstrates the plausibility of this concept. In individuals with a normal aortic valve, compensatory mechanisms can restore energetic balance during syncope. In contrast, only resting state is energetically stable in severe AS; all conditions involving low TPR are energetically unstable, regardless of compensatory response. As energy imbalance is incompatible with sustained cardiac function, it inevitably leads to death. The proposed mechanism does not require an exaggerated Bezold-Jarisch reflex, although this reflex likely acts as a trigger of syncope. Reference: Dvoulety, M. and Sitina, M. (2026), Haemodynamic-energetic mechanism of sudden cardiac death in severe aortic stenosis: A modelling study. J Physiol. https://doi.org/10.1113/JP288423

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Background: There is growing evidence of microcirculatory dysfunction being a major factor in determining the extent of multiorgan failure and, thus, the outcome of critically ill patients. Quick acidification of a bicarbonate anion (HCO₃⁻)-containing solution causes carbon dioxide (CO₂) supersaturation-triggered gas bubble formation in that solution. Blood is an HCO₃⁻-containing solution as well. Accordingly, we believe that the rapid occurrence of profound metabolic acidosis could result in gas bubble formation in the critically ill. Gas bubbles form due to CO₂ supersaturation at first, then other gases diffuse into bubbles in proportional amounts. Gas bubble-blood interface-triggered platelet adhesion and activation with consequent capillary occlusion could explain microcirculatory dysfunction. Methods: With a retrospective observational study including all admitted patients to our ICU in 2020, we investigated if there exists a correlation between the severity of metabolic acidosis in patients upon their admission to the ICU and their platelet count trend in the following two days. Base excess (BE) from blood gas analysis with the lowest pH around ICU admission was used as a marker of the severity of metabolic acidosis. Platelet counts in patients upon admission and lowest platelet count on their second day were used to calculate patients' relative platelet count decline after ICU admission; delta P = ((P2−P0)/P0) x 100. Results: Comparison of delta P in all six groups of BE showed a statistically significant difference (Kruskal–Wallis test; p < 0.001). Patients from groups with more negative BE values tend to have more negative delta P. Conclusions: Patients with more profound metabolic acidosis upon their ICU admission tend to have larger relative platelet count decline in the following days. Although in a very indirect way, these findings support our theory of gas bubble-blood interface-triggered platelet consumption with resulting microcirculatory dysfunction in most severely ill ICU patients. References: 1. Tachon G, Harrois A, Tanaka S, Kato H, Huet O, Pottecher J, Vicaut E, Duranteau J. Microcirculatory alterations in traumatic hemorrhagic shock. Crit Care Med. 2014;42(6):1433-41. doi: 10.1097/CCM.0000000000000223. 2. Merdji H, Levy B, Jung C, Ince C, Siegemund M, Meziani F. Microcirculatory dysfunction in cardiogenic shock. Ann Intensive Care. 2023;13(1):38. doi: 10.1186/s13613-023-01130-z. 3. den Uil CA, Lagrand WK, van der Ent M, Jewbali LS, Cheng JM, Spronk PE, et al. Impaired microcirculation predicts poor outcome of patients with acute myocardial infarction complicated by cardiogenic shock. Eur Heart J. 2010;31(24):3032-9. doi: 10.1093/eurheartj/ehq324. 4. Damiani E, Carsetti A, Casarotta E, Domizi R, Scorcella C, Donati A, et al. Microcirculation guided resuscitation in sepsis: the next frontier? Front Med (Lausanne). 2023;10:1212321. doi: 10.3389/fmed.2023.1212321. 5. De Backer D, Orbegozo Cortes D, Donadello K, Vincent JL. Pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock. Virulence. 2014;5(1):73-9. doi: 10.4161/viru.26482. 6. De Backer D, Donadello K, Sakr Y, Ospina-Tascon G, Salgado D, Scolletta S, et al. Microcirculatory alterations in patients with severe sepsis: impact of time of assessment and relationship with outcome. Crit Care Med. 2013;41(3):791-9. doi: 10.1097/CCM.0b013e3182742e8b. 7. Scardina P, Edwards MA. Prediction and measurement of bubble formation in water treatment. Journal of Environmental Engineering. 2001;127(11):968-73. 8. Levi M, Opal SM. Coagulation abnormalities in critically ill patients. Crit Care. 2006;10(4):222. doi: 10.1186/cc4975. 9. Pontier JM, Blatteau JE, Vallée N. Blood platelet count and severity of decompression sickness in rats after a provocative dive. Aviat Space Environ Med. 2008;79(8):761-4. doi: 10.3357/asem.2299.2008. 10. Pontier JM, Jimenez C, Blatteau JE. Blood platelet count and bubble formation after a dive to 30 msw for 30 min. Aviat Space Environ Med. 2008;79(12):1096-9. doi: 10.3357/asem.2352.2008. 11. Pontier JM, Vallée N, Bourdon L. Bubble-induced platelet aggregation in a rat model of decompression sickness. J Appl Physiol. 2009;107:1825-9. doi:10.1152/japplphysiol.91644.2008.

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INTRODUCTION: Acute right ventricular (RV) failure is a challenging condition in critical care associated with significant morbidity. Portopulmonary hypertension, a severe and under-recognized complication of liver cirrhosis, is an important cause of right-sided heart failure in chronic liver disease. We present the case of a 69-year-old female with cirrhosis who developed cardiac arrest secondary to acute decompensated right ventricular (RV) failure likely due to underlying portopulmonary hypertension. CASE REPORT: A 69-year-old female with Child Pugh B7 Hepatitis B cirrhosis and recurrent hepatic hydrothorax presented with syncope and exertional dyspnea. Imaging demonstrated a massive right pleural effusion, which was drained uneventfully. Computed tomography pulmonary angiography excluded pulmonary embolism but revealed right heart strain. The following day, while straining during defecation, she developed sinus bradycardia progressing to pulseless electrical activity arrest. Return of spontaneous circulation was achieved after 14 minutes. Bedside echocardiography demonstrated severe RV dilation with impaired systolic function (TAPSE 11 mm), septal flattening with left ventricular cavity obliteration, severe tricuspid regurgitation, and (estimated) elevated pulmonary vascular resistance. Lactate exceeded 10 mmol/L despite a preserved indirect Fick cardiac index, consistent with acute RV failure and mixed shock physiology. Acute decompensated RV failure, likely secondary to portopulmonary hypertension, was diagnosed. She required escalating vasopressor support and developed multi-system organ failure. Management targeted RV physiology: preload reduction with continuous renal replacement therapy, inotropic agents, pulmonary vasodilators, preferential vasopressin use, and ventilatory strategies avoiding high PEEP and hypercapnia. Despite transient echocardiographic improvement, she experienced recurrent arrests. Care was subsequently re-directed to palliation. CONCLUSION: This case underscores the importance of early recognition of RV-predominant shock physiology in cirrhosis and reinforces the need for timely identification of portopulmonary hypertension to mitigate the risk of acute decompensation.

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Introduction: Obesity-associated neuroinflammation is characterized by increased levels of saturated fatty acids (SFAs) and other lipids, along with the recruitment and activation of astrocytes and microglia, which actively contribute to the initiation and spread of the inflammatory response. Among the therapeutic strategies for obesity, glucagon-like peptide-1 (GLP-1) analogs have gained attention due to their anti-inflammatory, antidiabetic, and anti-obesity properties. This study aimed to investigate the effects of peripheral liraglutide treatment on lipid metabolism, mitochondrial function, and hypothalamic neuroinflammation induced by a high-fat diet (HFD). Methods: Male C57BL/6 mice were fed with either standard chow or HFD for 14 weeks. At the end of this period, the animals received daily injection of liraglutide(200 μg/kg, sc) for ten consecutive days. Body composition was assessed using the MiniSPEC NMR system before and after the treatment period. For histological analyses, immunofluorescence to detect hypothalamic and brainstem astrocyte activation through glial fibrillary acidic protein (GFAP) expression. The hypothalamic lipid profile was determined by high-performance liquid chromatography coupled with tandem mass spectrometry (LC–MS/MS), and mitochondrial function was assessed by high-resolution respirometry using the Oroboros O2k Oxygraph. Results: Liraglutide treatment significantly reduced food intake, body weight, fasting glucose levels, plasma triglycerides, total cholesterol, and leptin levels in HFD-fed mice (p < 0.05). In addition, liraglutide decreased both fat and lean mass (p < 0.05) and reduced GFAP expression in the hypothalamus and nucleus tractus solitarius (NTS). Furthermore, peripheral liraglutide administration altered the hypothalamic lipid profile and improved mitochondrial respiratory capacity (OXPHOS) in obese mice (p < 0.05; R²= 0.42). Conclusion: In conclusion, peripheral liraglutide treatment improves metabolic parameters, modulates hypothalamic lipid composition, enhances mitochondrial function, and attenuates hypothalamic neuroinflammation in diet-induced obese mice.

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Introduction Bioelectrical impedance analysis is a non-invasive method that evaluates body composition, cellular integrity, and hydration through phase angle1. While the relationship between phase angle and morbidity and mortality is well established in major surgeries with large fluid shifts. The effects of preoperative fasting, fluid restriction, and irrigation fluid absorption during transurethral resection on body fluid compartments ratio are unclear2-4. Although TUR is considered minor surgery, absorbed irrigation fluid may affect fluid distribution. This study aimed to evaluate the effects of perioperative fluid management on BIA parameters and phase angle in TUR patients. Methods This prospective study included 43 ASA I–III patients undergoing TUR surgery under general or spinal anesthesia. BIA measurements, including phase angle and body fluid compartments, were obtained preoperatively, in the early postoperative period, and at postoperative 24th hour. Intraoperative fluid management, anesthesia and surgical type, laboratory data, length of stay, and complications were recorded and analyzed using SPSS 27.0. Results: The mean age was 66.79±8.84 years, fasting time 12.9±2.25 hours, surgical duration 60.21±23.13 minutes, and irrigation volume 15,469±7,318 mL. No significant changes in fluid parameters were observed in the early postoperative period compared with preoperative values. However, significant differences were found at 24th hour. Diabetes mellitus was associated with changes in intracellular water, extracellular water, and phase angle at 24th hour. Other comorbidities, surgical type, and anesthesia method showed no significant differences. Diuretic use was associated with differences in preoperative and 24th hour phase angle. Conclusion Unlike sepsis, early-stage fluid shifts after TUR surgery were not evident with BIA5,6.Fluid distribution became more evident 24 hours after surgery; intracellular fluid decreased, while total and extravascular fluid increased. In patients with comorbidities and diuretic use, a PhA below 5° at 24 hours was associated with a risk of postoperative complications. Referances 1. Barbosa-Silva MCG, Barros AJD. Bioelectrical impedance analysis in clinical practice: A new perspective on its use beyond body composition equations. Curr Opin Clin Nutr Metab Care. 2005;8(3):311-317. doi:10.1097/01.mco.0000165011.69943.39 2. Chong JU, Nam S, Kim HJ, et al. Exploration of Fluid Dynamics in Perioperative Patients Using Bioimpedance Analysis. Journal of Gastrointestinal Surgery. 2016;20(5):1020-1027. doi:10.1007/s11605-015-3063-1 3. Asklöf M, Kjølhede P, Wodlin NB, Nilsson L. Bioelectrical impedance analysis; a new method to evaluate lymphoedema, fluid status, and tissue damage after gynaecological surgery - A systematic review. European Journal of Obstetrics and Gynecology and Reproductive Biology. 2018;228:111-119. doi:10.1016/j.ejogrb.2018.06.024 4. Cai B, Luo L, Zhu C, et al. Influence of body composition assessment with bioelectrical impedance vector analysis in cancer patients undergoing surgery. Front Oncol. 2023;13:1132972. doi:10.3389/fonc.2023.1132972 5. Kyosebekirov E, Kazakov D, Nikolova-Kamburova S, et al. Bioimpedance analysis for fluid status assessment in critically ill septic patients. Folia Med (Plovdiv). 2024;66(3):323-331. doi:10.3897/folmed.67.e125812 6. Madsen JM, Itenov TS, Koch EB, Bestle MH. Bioimpedance as a measure of fluids in patients with septic shock. A prospective observational study. Acta Anaesthesiol Scand. 2023;67(3):319-328. doi:10.1111/aas.14180

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Introduction: Clinicians use the standard base-excess (SBE) as a CO₂-independent marker of metabolic acid-base status. However, the reliance on a fixed non-carbonic buffer power (β = 16.2 mEq/L) may yield misleading results when concentrations of buffers (hemoglobin, albumin, and phosphate) and/or interstitial, plasma, and red-cell volumes are altered. We hypothesize that a measured, subject-specific extracellular base-excess better reflects the metabolic response to acute hypercapnia than SBE. Methods: Six female pigs were sedated and mechanically ventilated. Indocyanine green was used for plasma volume determination, and red-cell volume was subsequently derived from hemoglobin concentration. Extracellular fluid volume (ECF = plasma + red-cell + interstitial volume) was measured with bromide dilution. Respiratory acidosis was induced via controlled hypoventilation, with arterial gases assessed after 0, 20, 40, 60, 90, and 120 minutes. At the end, ascitic fluid was sampled for biochemistry as a surrogate for interstitial fluid, and the urinary catheter was voided to assess net acid excretion (NAE). Extracellular base excess (BE_ECF) calculated using measured compartment volumes and relative buffer concentrations was compared with SBE (Radiometer ABL90-FLEX). Results: For 54[45-60] kg body weight, plasma, interstitial, and ECF volumes were 1.71[1.43-2.05], 17.1[14.0-17.5] and 19.4[16-20] L, respectively. Plasma albumin and phosphate were 31.5[30.7-33.0] g/L and 3.3[3.2-3.5] mmol/L, with ascites-to-plasma ratios of 0.51[0.42-0.57] and 1.08 [1.06-1.11], respectively. Hemoglobin was 84[80-86] g/L. The resulting extracellular buffer power was 4.2[4.1-4.4] mEq/L. During hypercapnia (PCO₂ 37[36-38] to 103[97-106] mmHg, pH 7.52[7.51-7.53] to 7.13[7.1-7.15]), SBE decreased by 0.05[0.04-0.06] mEq/(L×mmHg) (∼ -3.1 mEq/L in total), p<0.01 , while BEECF increased by 0.014[0.00-0.03] mEq/(L×mmHg) (∼ +0.9 mEq/L in total), p=0.02. NAE was 21.3 [16.8-28.9] mEq, i.e. ∼1.1mEq/L of ECF. Conclusions: Subject-specific BE_ECF accurately reflects urinary acid excretion, while SBE erroneously indicates accumulation of metabolic acid during hypercapnia. Thus, SBE may be unreliable in patients with altered buffering capacity. Supported by grants NW26-01-00360 by Czech Health Research Council (AZV) and PRIMUS/26/MED/009 by Charles University.

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Background: Mechanical ventilation could affect the central venous pressure via changes in intrathoracic pressures. Objective: To predict the transmission ratio of the airway pressures changes on central venous pressure (CVP). Methods and analysis: A retrospective analysis of mechanically ventilated patients from the AmsterdamUMC ICU database was conducted. For each patient, variables describing mechanical ventilation (PEEP, DP, PPlat, I:E ratio, RR, VT, PAW mean) and CVP were extracted. These sub-sets were used to determine optimal combinations of input features for identifying nonlinear patterns. Exclusion criteria for the factors compromising the accuracy of central venous pressure measurements were applied. We applied XGBoost as a predictor, for its interpretable decision tree characteristics that captures non-linear relations well, as it harnesses methods to mitigate overfitting while training. It optimizes a global objective function combining a loss term and regularization to control model complexity. Using second - order gradient, tree splits are selected to maximize loss reduction while maintaining regularization. Trees are sequentially added with a learning rate to ensure stable model improvement and strong generalization. As a cross-reference means to study the generalization properties and mitigate overfitting with XGBoost, a two-stage predictor is set in a series of four ensemble based learners: XGBoost, LightGBM, CatBoost, and Random Forest to lend insights for change in performance and narrow the best performing method. Results and Discussion: The evaluation benchmarks of the models yielded sufficient accuracy, indicating its generalizability supporting its predictive capability to unseen samples. Studying the samples, we’ve noticed that not alone airway pressure has influence on venous pressure levels, yet also a small increase in PEEP contributes to increase in CVP Conclusions: Adjustments in mechanical ventilation parameters influence CVP. To support personalized approach, a data driven approximator was trained to predict CVP levels.

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Background Cardiopulmonary bypass-associated inflammation can produce mixed cardiogenic–vasodilatory shock, characterized by myocardial dysfunction and hypotension, often refractory to conventional vasoactive agents. We report successful rescue use of total plasma exchange (TPE) in three patients with this specific type of shock. Methods The first patient underwent CABG and PFO closure, and required the institution of V–A ECMO for separation from CPB, with pharmacological requirements reaching a peak Vasoactive-Inotropic Score (VIS) of 136. The second received aortic and mitral valve replacement for severe regurgitation secondary to infectious endocarditis; discontinuation of extracorporeal circulation was only achievable through VA–ECMO support amidst a profound catecholamine requirement, peaking at a VIS of 306. The third patient underwent aortic and mitral valve replacement for combined valvular stenosis. CPB separation was achieved with vasoactive support reaching a peak VIS of 78. Adjunctive therapy including hydrocortisone hemisuccinate and hydroxocobalamin 5g were uniformly administered across the entire patient series. Results Renal replacement therapy with an in-line hemadsorption filter was initiated upon admission of the first patient, with a suboptimal clinical response; given the persistent hemodynamic collapse, a salvage intervention with therapeutic plasma exchange was commenced. Serial IL-6 assays confirmed a marked reduction in the systemic inflammatory burden, with the expeditious down-titration of vasoactive support and the discontinuation of VA–ECMO. This prompted the early deployment of TPE in the subsequent cases, with comparable outcomes: a significant reduction in IL-6 assays and the concurrent weaning of multimodal vasoactive support to the point of sustained hemodynamic stability. Conclusion TPE provides a potentially effective salvage therapy for refractory post–cardiopulmonary bypass mixed shock, facilitating quantifiable humoral reset and rapid hemodynamic stabilization. Controlled studies are needed in order to formally define standardized indications, optimal timing and biomarker–guided endpoints.

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Background: The management of refractory status epilepticus (RSE) often requires high doses of sodium- channel blocking antiepileptics. While effective for seizure control, these agents, particularly phenytoin, are associated with significant cardiotoxicity. We report a case of severe cardiac conduction disturbances and hemodynamic instability following the administration of a multi-drug antiepileptic regimen. Methods:A 79-year-old female with a history of meningioma resection presented with focal-to-bilateral tonic-clonic SE. Initial management included 4g of levetiracetam, 20mg of diazepam, and 250mg of phenytoin. Due to persistent seizure activity, the patient was intubated and started on propofol and remifentanil sedation. Upon Intensive Care Unit (ICU) admission, an additional dose of phenytoin was administered, and maintenance therapy with levetiracetam (1g BID) was initiated. Empirical coverage with ceftriaxone and acyclovir was provided due to a recent history of a vesicular rash. Results: Within hours of ICU admission and following antiepileptic loading, the patient developed nystagmus and significant QTc prolongation, progressing to long QT syndrome accompanied by acute hemodynamic instability. Despite initial stabilization, the following day the patient manifested transient Mobitz Type II atrioventricular block. A temporary transvenous pacemaker was inserted; however, sinus rhythm was restored within the next hour. The patient was successfully weaned from mechanical ventilation and vasopressors, and subsequently transferred to the neurology ward. Maintenance therapy continued with phenytoin (125mg TID) and levetiracetam (1.5g BID). Regrettably, on the 38th hospital day, the patient died due to septic shock and multi-organ failure caused by a multidrug-resistant Gram-negative infection. Conclusion: This case highlights the critical need for continuous cardiac monitoring during the aggressive treatment of SE. The synergy of high-dose antiepileptics can trigger life-threatening arrhythmias and conduction blocks, even in patients without prior cardiac history. Clinicians must remain vigilant for iatrogenic cardiotoxicity, as these complications may necessitate invasive interventions.

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Background: Protective mechanical ventilation (PMV) is recommended in severe traumatic brain injury (TBI) due to increased risk of ventilator-induced lung injury and ARDS. However, low tidal volumes and higher PEEP may induce hypercapnia and impair cerebral venous drainage, potentially worsening secondary brain injury. Objective: Machine learning recognition of the interdependence between cerebral perfusion pressure and mechanical ventilation. Methods and materials: A retrospective analysis of TBI patients from the AmsterdamUMC ICU Database was conducted. Intracranial pressure (ICP) and cerebral perfusion pressure (CPP), along with mechanical ventilation parameters (PEEP, DP, Pplat, I:E ratio, RR, VT, Paw mean, FiO2, pO2, pCO2, P/F ratio) and central venous pressure, were extracted. These datasets were used to determine optimal combinations of input features for identifying nonlinear patterns. To model such time series rich data, we attempt to predict CPP recordings with a TCN-Transformer hybrid approach. It is an architecture that combines one-dimensional convolutional networks (CNN) and a parallel transformer. This pipeline model can process raw sequences to extract hierarchical temporal features and conveys the data to global relational mapping, which is suitable for processing of nonlinearity in bio-signals. Results and Discussion: Analysis of the available patient datasets suggests a seasonal inversely proportional trend in airway pressure levels and the corresponding cerebral perfusion levels during mechanical ventilation. Such a time series trend could be a subject of contribution to a secondary brain injury. The evaluation benchmarks of the deep learning model yielded sufficient accuracy, indicating its generalizability, supporting its predictive capability to unseen samples. Conclusions: Adjustments in PMV parameters may influence CPP and have clinically relevant effects on brain injury. To support personalized mechanical ventilation and make it protective not only to the lungs but also to the brain, a data driven approximator was trained to predict CPP and ICP levels.

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Background Microplastics and nanoplastics (MNPs) are pervasive environmental contaminants with potential human health implications. Although laboratory models implicate MNPs in oxidative stress, inflammation, and endocrine disruption, a comprehensive synthesis of direct in vivo human evidence is lacking. We aimed to systematically review studies measuring MNPs in living human subjects and summarise associated health findings. Methods We systematically searched PubMed, Web of Science, Scopus, Cochrane and Embase through 26 December 2024. Two investigators independently screened and selected original research articles that quantified MNPs in biological samples from living humans. We excluded animal, in vitro, cell-line, and injection-based studies, as well as reports on non-plastic micro- and nanoparticles. Data extraction, performed in duplicate, included study design, participant characteristics, detection methods, polymer types, and reported health outcomes. Methodological quality was appraised using Risk Of Bias in Non-Randomized Studies—of Exposures (ROBINS-E). The primary outcome was the presence and burden of MNPs; secondary outcomes were clinical or biomarker associations. No metaanalysis was performed due to heterogeneity. Results From 5 522 records, 25 studies met inclusion. Studies employed pyrolysis–gas chromatography/mass spectrometry (n = 9), Raman spectroscopy (n = 8), infrared spectroscopy (n = 7), and Fourier-transform infrared spectroscopy (n = 3), often combined with microscopy for MNP detection. Predominant polymers were polyethylene, polypropylene, polyvinyl chloride, polyethylene terephthalate, and polystyrene. In cardiovascular research (5 studies; n = 454), higher thrombus and plasma MNP burdens correlated with inflammatory markers and adverse cardiac events. Reproductive research (seven studies; n = 327) linked semen and tissue MNPs to reduced sperm quality and accumulation in tumor and placental samples. Gastrointestinal research (9 studies; n = 537) associated fecal MNPs with liver enzyme elevations and gut dysbiosis. Respiratory (3 studies; n = 171) and ocular (1 study; n = 49) research detected MNPs in airway fluids and vitreous humor respectively, with links to airway inflammation and increased intraocular pressure. ROBINS-E assessments indicated moderate to high risk of confounding and exposure-measurement bias; consistency across detection modalities was limited. Conclusion Human in vivo evidence confirms that MNPs accumulate in multiple organ systems and are associated with inflammation and functional impairment. Methodological heterogeneity and bias constrain causal inference. Prospective cohort studies with rigorous exposure assessment and confounder control are needed to advance understanding and guide policy.

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Background: Patients with hematological diseases admitted to the intensive care unit (ICU) represent a high-risk subgroup characterized by profound immunosuppression, disease-specific emergencies, and treatment-related toxicity. Despite advances in hematology and critical care, a lingering perception of poor prognosis may still influence ICU triage and escalation decisions. Objectives: To characterize the clinical profile, admission etiologies, organ support requirements, complications and outcomes of hematological patients admitted to a terciary ICU over 5 years, and to identify factors associated with mortality. Methods: We conducted a retrospective observational study including adult patients with hematological diseases admitted to a single tertiary ICU over five years. Baseline demographics, hematologic diagnoses, treatment lines, and illness-severity scores at admission were recorded. We analyzed causes for ICU admission, infectious complications and microbiology, hematologic emergencies, organ support therapies - including invasive mechanical ventilation (IMV), vasopressors, renal replacement therapy (RRT), and plasmapheresis. Primary outcomes were ICU and 28-day mortality; secondary outcomes included ICU readmission. Survivors and non-survivors were compared. Results: Ninety-four patients were included. The average age was 58.9 ± 15.2 years and 57% were male. Acute leukemias and aggressive lymphomas were the most frequent underlying diseases. Respiratory failure and sepsis were the leading causes of ICU admission. Gram-negative bacteria were the most frequently isolated pathogens, particularly Escherichia coli and Pseudomonas aeruginosa. More than 50% of the patients required IMV and most required vasopressor support.; a subset received RRT and plasmapheresis. ICU mortality was 35%, increasing to 56% at day 28. Non-survivors had higher severity scores, lower PaO2/FiO2 ratios, and required more invasive organ support. ICU readmission occurred in approximately 25% of cases. Conclusions: Critically ill patients with hematological diseases frequently present with infection-driven organ failure requiring aggressive organ support, yet meaningful survival is achievable even in severe cases. Outcomes appear primarily determined by the severity of acute organ dysfunction – particularly hypoxemic respiratory failure requiring IMV - rather than the underlying malignancy per se. These findings support early ICU involvement, proactive escalation of organ support and multidisciplinary management, reinforcing the concept of a distinct critical-illness phenotype within hematology.

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Introduction Emergency ultrasound has become fundamental for the management of critically ill patients. POCUS is commonly used in the emergency department (ED) because it allows rapid bedside diagnosis. Its utilization is increasing during cardiopulmonary resuscitation (CPR) and has the potential to improve Advanced Life Support (ALS) outcomes. Meanwhile, transesophageal echocardiography (TEE) has gained importance in critical care and may benefit the resuscitation of cardiac arrest for several reasons. Future research is warranted to confirm the added value of TEE in ALS and its clinical feasibility during CPR. Case presentation A 68-year-old man was admitted to our ED after out-of-hospital cardiac arrest. After breakfast and taking his antihypertensive medication, he developed sudden severe chest pain and collapsed when the Emergency Medical Services arrived. The first ECG showed pulseless electrical activity. ROSC was not achieved at home and the patient was intubated and transferred to hospital under mechanical chest compression device (“LUCAS”) and norepinephrine infusion. Bedside POCUS was inconclusive due to technical limitations and poor image quality, but raised suspicion for pericardial effusion. TEE was performed because the patient had a history of ascending aortic aneurysm. The mid-esophageal 2-chamber view demonstrated a severe (> 20 mm) loculated pericardial effusion along the anterior wall of the left ventricle (Figure 1A). The mid-esophageal long-axis view showed an intimal flap in the proximal ascending aorta, consistent with a Stanford Type A dissection (Figure 1B). Unfortunately, we only observed agonal twitching with no organized cardiac activity on ultrasound. Finally, considering persistent pulseless electrical activity with cardiac standstill, we decided to discontinue resuscitation efforts. Discussion Emergency ultrasound represents a fundamental skill in the current practice of emergency medicine. Recommendations for education, training experience and quality improvement in the emergency setting are well described in the literature. POCUS can reliably be used to identify reversible causes of CA [1]. However, POCUS use during cardiac arrest management may be associated with prolonged CPR pauses [2]. TEE could be used to diagnose reversible causes of collapse, optimize the quality of chest compressions, guide therapies, and identify cardiac activity [3]. Despite potential advantages during resuscitation, TEE is not currently widely adopted in the routine practice of ED. As described in the « 2025 European Resuscitation Council Guidelines », further studies are needed to better define the diagnostic value of TEE in identifying reversible pathology and myocardial contractility in cardiac arrest patients [4]. Development of a comprehensive guide is also essential to define the minimum training requirement for an effective implementation of TEE into emergency medicine practice. In the meantime, developing local CPR protocols in collaboration with TEE-proficient specialists may offer crucial information to physicians involved in cardiac arrest management (Figure 2). Conclusion Focused cardiac ultrasound during resuscitation represents an increasingly important skill for the modern critical care physician. Understanding cellular physiology and its integration into the management of cardiac arrest may facilitate decision-making during resuscitation. Our experience demonstrates that point-of-care TEE can be instrumental in the diagnosis and treatment guidance of cardiac arrest and acute aortic syndrome. Further studies are required to validate the clinical benefit and feasibility of implementing TEE during CPR.

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Introduction Mechanical circulatory support devices have become an integral component of modern cardiac intensive care, significantly improving survival in advanced heart failure. Implantation of a biventricular assist device (BiVAD) profoundly alters cardiovascular physiology, creating a state of device-dependent circulation in which pump flow, rather than intrinsic myocardial performance, determines cardiac output. With Frank–Starling mechanism no longer functioning adequately, and the presence of concomitant autonomic and endothelial dysfunction, the heart’s capacity to respond to physiological stressors is substantially compromised. In this context, the onset of septic shock may generate metabolic and hemodynamic demands that exceed the adaptive capacity of device-supported circulation. Methods We analyzed the pathophysiological mechanisms underlying septic shock in BiVAD supported patient, with particular focus on hemodynamic responses to pump flow adjustments and on laboratory parameters reflecting tissue perfusion, inflammation, and organ dysfunction. In order to respond to the higher metabolic needs and improve the systemic perfusion an echocardiography-guided optimization of BiVAD pump parameters was performed. Results In BiVAD-supported patients, the increased metabolic and circulatory demands associated with sepsis cannot be adequately met due to limited or absent native cardiac reserve. Compensatory mechanisms as tachycardia and enhanced myocardial contractility are absent or markedly blunted. Moreover, the absence of pulsatile blood flow leads to impaired regulation of vascular tone. This results in a dissociation between pump flow, arterial pressure, and tissue perfusion. Sepsis-induced systemic vasodilation further aggravates the imbalance between fixed or semi-fixed cardiac output and reduced systemic vascular resistance, creating a complex hemodynamic state characterized by features of both cardiogenic and distributive shock. Even though an integrated therapeutic approach incorporating pump flow optimization and multimodal organ support in this case was associated with favorable clinical outcome, the treatment is significantly prolonged. Conclusion The coexistence of constrained cardiac output and sepsis-induced vasodilation in a patient supported with BiVAD produces a mixed form of cardiogenic and distributive shock with impaired compensatory mechanisms. Recognition of this unique hemodynamic profile is essential for appropriate monitoring and therapeutic strategies. To achieve a hyperdynamic response, a multimodal management strategy is required, in which pump flow may be adjusted, with careful consideration of the associated risk of suction events.

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Abstract Background: Hyponatremia is a common feature of severe hyperglycemia in diabetic patients. We studied whether it is due to plasma dilution, a sodium deficit, or both. Methods: In 17 patients with diabetes-induced severe hyperglycemia, blood hemoglobin and the concentrations of glucose, sodium, and other electrolytes in plasma and urine were measured during and after an intravenous infusion of 1 L of 0.9% saline over 30 min on two consecutive days. Fluid volume and electrolyte kinetics were applied to study relationships between the glucose and electrolyte levels and to estimate the sizes of the body fluid compartments. Results: There was a statistically significant inverse linear relationship between plasma glucose (highest value 53 mmol/L) and plasma sodium (lowest 120 mmol/L). The correction factor was 1.6 or 2.2 depending on how the comparison was made. The hyperglycemia on admission corresponded to a fluid shift from the intracellular space of 350 mL, which was sufficient to explain the difference in baseline plasma sodium between the two study days. However, this dilution co-existed with a 20% reduction of the plasma and extracellular fluid volumes, and the body contents of sodium and chloride were 26% and 30% below normal, corresponding to deficits of 400 mmol. Restoration of the acid-base balance and the kidney function, rather than decreasing plasma glucose levels, seemed to drive the normalization of plasma sodium. Conclusions: Hyponatremia in severe diabetic hyperglycemia can be explained both by dilution and a sodium deficit. The medical treatment should consider both factors. Keywords: Dehydration, diagnosis, urine, physiopathology, diabetes mellitus, physiology; normal saline; pharmacokinetics.

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Background: Ventilator-induced lung injury (VILI) remains a major challenge associated with mechanical ventilation. A primary mechanism underlying VILI is cyclic alveolar recruitment and derecruitment (R/D) (atelectrauma). To minimise its development, ventilator settings, such as Positive End-Expiratory Pressure (PEEP), must be carefully optimised for each patient. Despite this need for personalisation, current bedside techniques cannot continuously measure local alveolar dynamics. Consequently, clinicians must rely on global parameters, which may not fully capture the heterogeneity of regional lung behaviour. In silico modelling offers a promising solution by linking local alveolar mechanics with global lung function. We sought to investigate whether our in silico modelling framework could simulate the effect of an impaired lung on R/D behaviour. Methods: This work leverages a lumped-parameter model presented in [1], which estimates patient-specific regional elastance and recruitment information derived from dual-volume CT in a mechanically ventilated ARDS patient. The model was used to simulate mechanical ventilation during an incremental PEEP trial consisting of 30-second steps at 5, 10, and 15 cmH2O. Next, the mean critical pressures were shifted by +5cmH2O to mimic a severe lung injury, and the trial was repeated. Results: The shifted-critical-pressures trial demanded higher PEEP to maintain alveolar aeration throughout the respiratory cycle. It was observed that tidal recruitment remained high and unstable at 10cmH2O and was significantly reduced only at the higher PEEP of 15cmH2O, while it was already reduced at 10cmH2O in the control simulation. Conclusion: In this study we utilised a methodology that infers local lung properties derived from dual-volume CT. A proof-of-concept simulation shows that the model can reproduce the effect of conventional changes in ventilator settings, such as PEEP, as well as can simulate an impaired lung with worsening biomechanics. As such, this scalable strategy provides a mechanistic foundation for future personalised ventilator optimisation to reduce atelectrauma. References [1] Quicken et al., ESB 2025 conference.

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Introduction: Post-Hypoxic Myoclonus (PHM) can present early after cardiac arrest and indicates poor neurologic outcome. Its management may be challenging and EEG may aid to guide clinical management. We present the management of a patient suffering from acute, persistent PHΜ in absence of bedside EEG. Methodology: This is the case of a 46 year old man who survived after cardiac arrest due to a STEMI. After primary PCI the patient was initially admitted in the Coronary Care Unit, intubated under sedation with propofol infusion. Shortly after cessation of the sedative medication he developed bilateral asymmetrical (right prominent side) myoclonus of the limbs which was treated with levetiracetam. A brain CT was performed which revealed diffuse brain edema and then at day 4 the patient was transferred to the ICU for further management under sedation with propofol, fentanyl and midazolam continuous infusion. Mannitol was also administered and sedation was withheld after 48 h to allow for assessment of the neurologic status. Myoclonus was evident within 15 minutes, sedation was reinitiated and valproic acid as a continuous infusion was added along with an increase of levetiracetam. The following days as guided by neurologic consultation, antiepileptic medication had to be titrated until day 23 due to persistent myoclonus activity up to levetiracetam 6g, valproic acid 4g, clonazepam 3mg, lacosamide 200mg and perampanel 8mg. He also received continuous infusion of 1.5mg/kg/h ketamine for 24 hours to allow for therapeutic levels of the accompanying treatment. Management of antiepileptic medication was based on clinical manifestations of myoclonus due to lack of portable EEG. Results: On day 23 of hospitalisation the patient status allowed for his transfer to the EEG laboratory where despite demonstrating myoclonus, this was not associated with epileptiform abnormalities in the EEG. The EEG performed was asymmetrical, with θ waves in the left hemisphere, lack of basal activity was recorded in the other hemisphere and myoclonic status epilepticus of cortical origin was excluded. Gradually, the frequency of myoclonus decreased and antiepileptic treatment was reduced to 2.4g valproic acid, lacosamide 100mg, clonazepam 1mg, perampanel 8mg and levetiracetam 4g. No ECG changes were recorded during the course of treatment. The patient died after 58 days of hospitalisation due to complications of sepsis. Conclusion: PHM can be a challenging phenomenon that occurs after cardiac arrest. EEG data may not be indicative of clinical manifestations while thorough, step by step titration is necessary to manage such demanding and persistent cases.

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Introduction: Renal compensation for respiratory acidosis develops over hours to days, yet its onset and mechanisms remain poorly defined. We hypothesize that an immediate decrease in urinary strong ion difference (SIDu) generates an equivalent net acid excretion (NAE). Methods: Six female pigs were sedated and mechanically ventilated. Respiratory acidosis was induced by controlled hypoventilation over 120 minutes. Urine was analyzed for phosphate and creatinine concentrations then collected every 20 minutes for Na⁺, K⁺, Cl⁻, pH, ammonium and urinary volume measured via the KING (Kidney Instant Monitoring). SIDu was calculated as Na⁺ + K⁺ - Cl⁻, NAE as ammonium + titratable acidity (protons bound by phosphate and creatinine) - bicarbonate. Areas under the curves (AUC) of ∆SIDu and ∆NAE vs cumulative urine volume were compared as measures of total excreted acidity. Results: During 2 hours of hypercapnia (PCO₂ 37 [36; 38] to 103 [96; 106] mmHg, pH 7,52 [7,50; 7,53] to 7,12 [7,10; 7,13]), the kidney produced 376 [331; 425] ml of urine. The renal response (urinary pH 7,40 [6,86; 7,44] to 4,69 [4,65; 4,85] mEq/L) was detectable within the first 20 minutes and was characterized by a drop in SIDu (106,2 [60,9; 160,6] to 29 [9,3; 30,1]), mainly mediated by a decrease in urinary potassium (Figure 1). NAE went from negative values (-18.6 [-24,5; -2,6] mEq/L) reflecting bicarbonate generation at high urinary pH, to 70.3 [62,5; 80,9] mEq/L through bicarbonate reabsorbtion, ammonium generation, and increased titratable acidity (Figure 1). AUCs of ΔSIDu and ΔNAE did not differ (23,8 [13,0; 16,1] vs 21,3 [16,8; 28,9] mEq, p = 0,84). Conclusions: Acute hypercapnia triggers immediate renal response, with rapid urine acidification due to decreasing SIDu allowing for net acid excretion. Tight coupling of ΔSIDu and ΔNAE suggests that lowering urinary SID is the main mechanism enabling renal acid elimination through urinary buffers.