Search Results (112)

Acute hypoxemic respiratory failure (AHRF) represents one of the most common and clinically challenging indications for invasive mechanical ventilation in the intensive care unit, characterized by profound etiological heterogeneity that demands accurate diagnosis to guide treatment. While clinical history, physical examination, and laboratory data remain essential, they are often insufficient to reliably discriminate among conditions such as acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, and pneumonia—particularly in mechanically ventilated patients. Lung imaging has therefore emerged as an indispensable complement to clinical assessment. In this narrative review, we systematically describe the physical principles, clinical applications, and limitations of the imaging modalities currently available in critical care: chest X-ray (CXR), computed tomography (CT), lung ultrasound (LUS), electrical impedance tomography (EIT), and positron emission tomography (PET). CXR remains the most widely used bedside tool but is constrained by low sensitivity and significant interobserver variability. CT is the gold standard for morphological and quantitative lung phenotyping, enabling the assessment of recruitability, baby lung characterization, and the identification of complications, but requires patient transport and exposes patients to ionizing radiation. LUS offers real-time, bedside evaluation of aeration with high diagnostic accuracy for pneumothorax and pleural effusion, and is increasingly integrated into revised ARDS diagnostic criteria. EIT enables continuous, radiation-free monitoring of regional ventilation distribution and positive end-expiratory pressure (PEEP)-guided titration directly at the bedside. While PET provides unparalleled quantification of regional inflammation and ventilation-perfusion mismatch, it currently remains a purely investigative research tool. Finally, we discuss emerging technological and AI-driven advances—including dual-energy CT, next-generation EIT, and deep learning algorithms—that are poised to transform lung imaging from a passive diagnostic tool into an active, personalized guide to respiratory management. Full article

Background: Magnetic particle imaging (MPI) is an emerging, tracer-based modality that directly detects superparamagnetic iron oxide nanoparticles (SPIONs) with exceptional sensitivity, quantitative signal behavior, and full immunity to air–tissue susceptibility artifacts. These features make MPI particularly well-suited for pulmonary imaging, where traditional techniques such as computed tomography (CT), magnetic resonance imaging (MRI), and nuclear medicine-based ventilation/perfusion (V/Q) imaging are limited by radiation exposure, low contrast, and motion-related signal degradation. Objective: This review synthesizes the current state of MPI for lung imaging, with emphasis on its physical principles, tracer development, preclinical applications, and its potential role in assessing pulmonary perfusion, vascular integrity, inflammation, and therapeutic responses. Methods: A systematic evaluation of preclinical studies was performed across three major application domains: pulmonary perfusion mapping, cell tracking and therapeutic monitoring, and vascular injury and permeability assessment. Study designs, SPION formulations, MPI acquisition strategies, and validation methods, including histopathology, biodistribution, broncho-alveolar lavage fluid (BALF) analysis, and Evans Blue assays, were examined to characterize methodological consistency and imaging performance. Results: MPI consistently demonstrated high-contrast, quantitative visualization of pulmonary blood flow, endothelial barrier disruption, inflammatory signaling, and transplanted or inhaled cell populations. Tracer engineering played a critical role: macroaggregated albumin superparamagnetic iron oxide nanoparticles (MAA-SPIONs) enabled capillary-level perfusion mapping, LS-008 improved temporal resolution and vascular delineation, Synomag/Synomag-D allowed quantification of vascular leakage in acute and chronic lung injury, and vascular cell adhesion molecule-1 (VCAM-1)-targeted probes provided molecular-level assessment of inflammation. Hybrid MPI-CT and MPI-MRI approaches further enhanced anatomic localization and enabled accurate pulmonary blood volume (PBV) estimation. Across studies, MPI measurements showed strong agreement with established biological assays and remained free of the artifacts that limit CT and MRI in the lung. Conclusions: Preclinical evidence demonstrates that MPI is a robust, radiation-free, and quantitatively precise modality for functional and molecular lung imaging. Its ability to map perfusion, track therapeutic agents, and noninvasively quantify vascular permeability positions MPI as a promising future alternative or complement to CT, MRI, and nuclear medicine for pulmonary assessment. Continued tracer optimization, system scaling, and clinical validation are key steps toward translating MPI into routine clinical use. Full article

Electrical impedance tomography (EIT) is a promising imaging tool in critical care. Its capacity to provide noninvasive bedside visualization of regional ventilation and perfusion with high temporal resolution makes it an ideal monitoring modality for patients on ventilation. However, its widespread implementation has been hindered by physical limitations in spatial resolution and a lack of robust evidence linking its use to improved clinical outcomes. In recent years, the commercialization of several bedside devices has led to growing clinical experience, gradually yielding concrete evidence regarding its clinical utility. Furthermore, beyond respiratory monitoring, data are increasingly accumulating in non-pulmonary fields, including perfusion, neuro-critical care and gastroenterology. Therefore, the objective of this review is to synthesize emerging evidence regarding the recent clinical applications of electrical impedance tomography and discuss future perspectives. Full article

Background/Objectives: The renal resistive index (RRI) has emerged as an early marker of renal vascular resistance. The purpose of this study was to investigate the association between RRI on intensive care unit (ICU) admission and the development of acute kidney injury (AKI) in a general ICU population, and to assess its predictive accuracy. Methods: This prospective observational study was conducted in a multidisciplinary ICU. Consecutive mechanically ventilated adults were enrolled; RRI was measured within 24 h of admission after hemodynamic stabilization. AKI was defined by Kidney Disease: Improving Global Outcomes (KDIGO) criteria within seven days. Multivariable regression, receiver operating characteristic (ROC), reclassification, and mediation analyses were performed. Results: A total of 181 patients were included. AKI occurred in 36%. Median RRI was 0.73 (0.65–0.80). RRI correlated with age, acute physiology and chronic health evaluation (APACHE) II and sequential organ failure assessment (SOFA) scores, lactate, and glomerular filtration rate (GFR) (all p < 0.001). In multivariable analysis, RRI was the only independent predictor of AKI (OR 2.86 per 0.05 increase, 95% CI 1.64–4.98, p = 0.001). It was also associated with an increased likelihood of presenting with a more severe AKI stage. RRI showed high discriminative ability (AUC = 0.89, 95% CI 0.84–0.94); the optimal cut-off was 0.77 (sensitivity 0.83, specificity 0.82). Adding RRI to a clinical model improved prediction (ΔAUC p = 0.049; net reclassification index (NRI) = 0.52, p < 0.001). Mediation analyses showed that RRI significantly mediated the effects of hypertension and low baseline GFR on AKI risk. Subgroup analyses confirmed consistent predictive performance across age, lactate, and sepsis categories. Conclusions: RRI is an independent early predictor of AKI and its severity, as well as a mediator of both hypertension and low GFR, regarding their effect on AKI development in ICU patients. RRI could serve as an early bedside marker of renal perfusion impairment in critically ill patients, guiding strategies aimed at reducing the risk of AKI. Full article

Introduction: Severe traumatic brain injury (sTBI) frequently coexists with polytrauma and often necessitates damage control neurosurgery (DCNS), where rapid decompression and temporary stabilization take precedence over definitive reconstruction. Within this context, anesthetic management must balance cerebral protection with ongoing resuscitation, yet high-quality DCNS-specific evidence remains limited. Materials and Methods: A comprehensive search of PubMed, Scopus, and Google Scholar (2015–2025) was conducted using MeSH terms and keywords related to neurotrauma, anesthesia, intracranial pressure, and perioperative management. Studies were included if they examined anesthetic or hemodynamic strategies in severe TBI or DCNS and reported relevant clinical or physiologic outcomes. Results: Nineteen articles addressing perioperative strategies for optimizing DCNS outcomes were analyzed. Discussion: Preoperative care emphasizes hemodynamic stabilization and permissive hypertension, damage control resuscitation including massive transfusion protocols, optimization of cerebral perfusion pressure (CPP) and neuromonitoring, and the use of hyperosmolar therapy. Transexamic acid can be used in sTBI safely but with unclear improvement in outcomes. Intraoperatively, propofol-based total intravenous anesthesia is generally preferred over volatile agents due to favorable effects on intracranial pressure (ICP), cerebral blood flow (CBF), autoregulation, and emergence. While historically contraindicated, ketamine and etomidate are now increasingly used as hemodynamically protective induction agents. Analgesic and sedative strategies prioritize dexmedetomidine and carefully titrated opioids to minimize respiratory depression and reduce postoperative complications. CPP and ICP-directed management relies on individualized blood pressure targets, vasopressor selection, lung-protective ventilation, and strict temperature control. Conclusions: Emerging evidence has suggested the benefit of DCNS for patient survival. Overall, perioperative care is guided largely by physiology and extrapolation, highlighting the need for standardized protocols. Full article

Background/Objectives: Pressure injuries on the heels of critically ill patients occurring during hospitalization are a global problem. Risk factors include comorbidities, distal perfusion disorders, multiple organ failure, pharmacotherapy, and immobilization associated with mechanical ventilation. These factors affect microperfusion quality in the heels. The presence of friction, shear, and compressive forces contributes directly to local tissue hypoxia and secondary tissue destruction in the heels. This study aimed to assess the impact of risk factors on the development of pressure injuries on the heels of patients in intensive care. Methods: A prospective observational study using controlled observation and assessment was conducted on 120 patients treated in the Department of Anesthesiology and Intensive Care. The initial risk assessment for pressure injuries was conducted within 24 h of admission to the ward, with a follow-up assessment conducted between five and ten days after admission. Data were collected using a scientific research protocol consisting of three parts (A, B, and C). Part A contained sociodemographic data, selected biochemical results, an ankle-brachial index assessment, and a pressure injury risk assessment using the Braden scale within the first 24 h of admission. Parts B and C involved re-evaluating selected biochemical parameters and assessing areas particularly vulnerable to pressure injury development. Statistical analysis was performed using IBM SPSS Statistics v. 21. Results: It was shown that the high risk of pressure injuries in the heel area in critically ill patients is dependent on catecholamine infusion (p < 0.001, r = 0.45) and distal perfusion dysfunction, which is assessed using the ankle-brachial index (ABI-PAD) (p = 0.026, r = 0.23). The ABI (PAD) index is an important factor in the development of pressure ulcers associated with peripheral artery disease, which is associated with an approximately fivefold increase in the likelihood of heel pressure injuries compared to patients with normal ABI values (OR = 5.10, 95% CI: 1.56–16.65, p = 0.007). A correlation was demonstrated between CRP values (chi-square = 5.795, df = 1, p = 0.016) and creatinine levels (chi-square = 7.512, degrees of freedom = 2, p = 0.023, r = 0.25) and the occurrence of pressure ulcers in the heels of critically ill patients. It was shown that the strongest prognostic factor for the occurrence of heel pressure injury was a below-normal creatinine level (OR = 8.75, 95% CI: 1.20–64.13, p = 0.033). Conclusions: Distal perfusion disorders resulting from circulatory failure and low peripheral perfusion increase the risk of pressure ulcer development in critically ill patients. The use of catecholamines to stabilize the circulatory system increases the risk of pressure ulcers on the heels of critically ill patients. Specific pharmacotherapy and invasive medical procedures may contribute to the development of pressure ulcers regardless of the level of pressure ulcer prevention. Full article

Background/Objectives: Molecular hydrogen (H₂), a natural antioxidant, can selectively reduce hydroxyl radicals and peroxynitrite without affecting signaling molecules such as H₂O₂ and NO. In addition, H₂ can inhibit the synthesis of inflammatory cytokines. Human and animal studies have shown that the inhalation of H₂ has a hypotensive effect. In this context, the aim of the present work was to study the effect of H₂ on the baroreflex regulation of blood pressure in rats with experimental monocrotaline-induced pulmonary hypertension (MCT) in vivo and the effects of H₂ on the reactivity of isolated rat aorta with MCT pulmonary hypertension to α₁-adrenoceptor agonists in vitro. Methods: Experiments were performed on male Wistar rats with MCT pulmonary hypertension; animals were placed in plastic chambers aerated with atmospheric air at a rate of 4 L/min with O₂ and CO₂ control. Cages with the rats of the MCT-H₂ and Control-H₂ groups were ventilated with air containing 4% H₂ twice daily for 2 h each. The MCT-Air and Control-Air groups breathed only atmospheric air. The duration of the experiment was 21 days. On day 20, blood pressure and heart rate (HR) were measured in awake animals and the baroreflex response to phenylephrine (PE) and nitroprusside (NP) was tested. In in vitro experiments, we studied the effect of adding H₂ to the perfusion solution on the responsiveness of isolated aortic preparations from MCT and control rats to the α₁-adrenoceptor agonist PE and the vasodilators NP and Acetylcholine. Results: When the effect of H₂ on the baroreflex response to NP (4.5 μg/kg) was examined in awake rats, the increase in HR was 73.1 ± 16.7 beats/min in the MCT-Air group and 48.1 ± 10.2 beats/min in the MCT-H₂ group (p < 0.01). In the Control-H₂ and Control-Air groups, there was a trend towards a lower HR in the Control-H₂ group, but the differences were not significant. No differences in HR response to PE administration were found between any of the experimental groups. Experiments on isolated aortic preparations from MCT rats showed that the addition of H₂ to the perfusion medium resulted in a 30% reduction in the maximal response to PE compared with the MCT group without hydrogen (p < 0.01), and the potency of PE (EC₅₀) decreased threefold (p < 0.05). There was a decrease in tryptase secretion, indicating an anti-inflammatory effect of H₂. Conclusions. The results demonstrate that H₂ inhalation was associated with an attenuated heart rate response to nitroprusside-induced hypotension and reduced vascular reactivity to phenylephrine in rats with pulmonary hypertension. Full article

Hypoxic pulmonary vasoconstriction (HPV) is a rapid and reversible constrictor response of the pulmonary vasculature, and especially its small muscular precapillary arteries, which is initiated by episodes of local alveolar hypoxia. Acting as a protective homeostatic vasomotor mechanism, HPV enables maximal gas exchange by diverting blood from poorly ventilated alveoli into those rich in oxygen, thereby optimizing oxygen uptake and the ventilation–perfusion (V/Q) ratio so as to maintain the arterial oxygen partial pressure (P_aO₂) within the physiological range. HPV is an intrinsic mechanism of pulmonary artery smooth muscle cells (PASMCs), and requires an O₂ sensor which acts through mediator(s) to trigger effector mechanisms within these cells to evoke constriction. Whereas HPV effector mechanisms are reasonably well defined, the nature of the O₂ sensor and mediators remains in dispute, and a number of proposals have been developed to account for these. Some (but not all) of these share a focus on the concept that hypoxia activates effector mechanisms by inducing a change in the PASMC cytoplasmic redox state. Of these, the Redox Theory, first proposed by Kenneth Weir and Stephen Archer in 1995, proposes that hypoxia inhibits mitochondrial production of reactive oxygen species (ROS), thereby causing the cytoplasm to become more reduced. This inhibits ongoing vasorelaxation maintained by the opening of voltage-gated K⁺ channels. In contrast, according to the Mitochondrial ROS hypothesis, introduced by Paul Schumacker and Naveen Chandel in 2001, hypoxia increases mitochondrial ROS production, causing an oxidizing shift in the cytoplasmic redox state that activates several vasoconstricting pathways. In a third redox-based scenario, developed by Michael Wolin and Sachin Gupte, hypoxia evokes contraction by causing a fall in H₂O₂ production by NADPH oxidase and by activating the pentose phosphate pathway. These effects inhibit basal vasorelaxation maintained by the guanylate cyclase and protein kinase G and also stimulate vasoconstricting mechanisms. In this comprehensive review, we first provide a detailed summary of the key studies contributing to the development of these proposals and then subject the evidence supporting them to a critical appraisal, based in part on how well they accord with the wider literature and recent developments in our understanding of how cells shape and deploy redox mechanisms in order to regulate cell function. Full article

Objectives: This study aims to evaluate whether changes in perfusion index (PI) after the first deflation of the blood pressure cuff during remote ischemic conditioning (RIC) are associated with passive leg raising (PLR)-induced changes in stroke volume. In addition, we compared PI changes after cuff deflation during RIC between critically ill patients and healthy controls. Methods: This prospective, single-center study was conducted in a mixed ICU at a tertiary teaching hospital. Patients aged >18 years admitted to the ICU, monitored using calibrated pulse contour analysis, and scheduled for a PLR test as decided by the attending physicians were included. The PI was measured after blood pressure cuff deflations during RIC (3 cycles of brachial cuff inflation to 200 mmHg for 5 min, followed by instantaneous deflation to 0 mmHg for another 5 min) in the supine position after PLR. Preload responsiveness was defined as a ≥10% increase in the stroke volume index (SVI) during PLR. Data were compared with a healthy control group. Results: Thirty-three patients were included (median age 62; 45% in shock; 55% mechanically ventilated). When comparing critically ill patients with healthy volunteers, the maximum PI change (dPImax) and the time to reach it were higher in critically ill patients after the first and second cuff deflations (p < 0.05). However, after the third deflation, the difference was no longer significant. Following the first deflation, dPImax was significantly correlated with SVI changes during PLR (r = 0.63, p < 0.001). After the cuff was first deflated, we detected a PI cutoff with a positive SVI response (≥10%) during PLR, with a sensitivity of 64% and a specificity of 94% (area under the receiver operating characteristic curve 0.752; 95% CI, 0.564–0.940; p = 0.008). Conclusions: The maximum change in perfusion index following brachial blood pressure cuff deflation after five minutes of inflation may serve as a promising noninvasive bedside indicator of preload responsiveness in critically ill patients. Additionally, the observed normalization of PI kinetics during RIC suggests possible acute modulation of vascular reactivity, though further research is needed to confirm an association between PI changes and endothelial function. Full article

Excessive right heart load imposes an acute or chronic injury on the right ventricle (RV), predisposing critically ill neonates and cardiac surgical patients to RV failure, low cardiac output syndrome, and death. Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator that improves ventilation–perfusion matching and unloads the RV without systemic hypotension; nonetheless, its application beyond established neonatal indications remains contentious. Our review synthesizes current mechanistic, translational, and clinical evidence regarding iNO use in three major settings characterized by excessive RV load: (1) neonatal pulmonary hypertension, particularly PPHN; (2) acute and chronic RV overload in older children and adults, including secondary pulmonary hypertension, acute respiratory distress syndrome (ARDS), and acute pulmonary embolism; and (3) perioperative and post-cardiopulmonary bypass (CPB) management in congenital and adult cardiac surgery. In term and near-term infants with hypoxic respiratory failure, pivotal randomized trials show that iNO consistently improves oxygenation and reduces extracorporeal membrane oxygenation (ECMO) use, but this has little effect on survival and long-term neurodevelopment. In ARDS and other adult critical-care indications, iNO provides transient improvements in gas exchange and RV performance without reducing mortality or ventilator duration, and meta-analyses signal an increased risk of acute kidney injury, particularly with prolonged use. In contrast, perioperative studies around CPB demonstrate that prophylactic postoperative iNO and intra-CPB nitric oxide administration can attenuate pulmonary hypertensive crises, facilitate separation from CPB, shorten ventilation and intensive care stay, and, in selected high-risk cohorts, may reduce cardiac surgery-associated acute kidney injury, although survival benefits remain unproven. Across these scenarios, iNO should be used judiciously and in a pathophysiology-driven manner as a time-limited, targeted adjunct to stabilize patients with documented or anticipated RV strain rather than a disease-modifying therapy. Future work should refine patient selection, timing, dosing, and weaning strategies, and define the long-term safety and cost-effectiveness of iNO within contemporary multimodal RV support pathways. Full article

Background: Long-term cognitive impairment is common among ICU patients who required invasive mechanical ventilation (IMV). Its etiology is likely multifactorial. This preregistered study examined the association between the duration of IMV and cognitive function post-ICU, as well as the moderating effects of age and cognitive reserve. Methods: A secondary analysis was conducted using data from a published study of COVID-19 ICU survivors. One year after discharge, participants underwent a neuropsychological assessment. Linear regression models were used to evaluate associations between the variables. Results: Among patients who received IMV via endotracheal intubation, ventilation duration was not significantly associated with cognitive performance. In contrast, among tracheostomized patients, longer IMV duration was associated with better cognitive outcomes (Cohen’s f² = 0.21). Age had a small negative main effect; in combination with IMV duration, f² increased to 0.31. Cognitive reserve showed a strong positive association with cognitive outcome; in combination with IMV duration, f² increased to 0.67. The interaction terms were negligible in both cases. Conclusions: We hypothesize that, compared to endotracheal intubation, IMV via tracheostoma may not only reduce the need for sedation, but also provide a more efficient respiratory support, therefore contributing to positive cognitive outcomes. However, IMV via tracheostomy still represents a form of positive pressure ventilation (PPV), which carries risks, such as ventilator-induced lung injury and reduced cardiac output and brain perfusion. These concerns about PPV, combined with our findings, indicate that alternative, non-invasive modes, such as negative pressure ventilation (NPV), warrant evaluation in future trials. Full article

Background and Objectives: Acute respiratory failure (ARF) has a heterogeneous course in the emergency department (ED), and early prediction of noninvasive mechanical ventilation (NIMV) failure is difficult. The PaCO₂–ETCO₂ gap reflects ventilation–perfusion mismatch and increased physiologic dead space; however, the prognostic value of its short-term change during NIMV is unclear. This study evaluated baseline, post-treatment, and delta (post–pre) PaCO₂–ETCO₂ gap values for predicting intubation, intensive care unit (ICU) admission, and mortality in ED patients with ARF receiving NIMV. Materials and Methods: This prospective observational study enrolled adults (≥18 years) treated with NIMV in a tertiary ED. Exclusion criteria included GCS < 15, intoxication, pneumothorax, trauma, pregnancy, gastrointestinal bleeding, need for immediate intubation/CPR, or incomplete data. ETCO₂ was recorded within the first 3 min of NIMV and at 30 min; concurrent arterial blood gases provided PaCO₂. The PaCO₂–ETCO₂ gap was calculated at both time points and as delta. Outcomes were intubation, ICU admission, and mortality. ROC analyses determined discriminatory performance and cutoffs using the Youden index. Results: Thirty-four patients were included (50% female; mean age 73.26 ± 10.07 years). Intubation occurred in 9 (26.5%), ICU admission in 20 (58.8%), and mortality in 10 (29.4%). The post-treatment gap and delta gap were significantly higher in intubated patients (p = 0.007 and p = 0.001). For predicting intubation, post-treatment gap > 10.90 mmHg yielded AUC 0.807 (p = 0.007; sensitivity 77.8%, specificity 76.0), while delta gap > 2.90 mmHg yielded AUC 0.982 (p = 0.001; sensitivity 88.9%, specificity 92.0). Delta gap also predicted ICU admission (cutoff > 0.65 mmHg; AUC 0.746, p = 0.016) and mortality (cutoff > 2.90 mmHg; AUC 0.865, p = 0.001). Conclusions: In ED ARF patients receiving NIMV, an increasing PaCO₂–ETCO₂ gap—especially the delta gap—was associated with higher risks of intubation, ICU admission, and mortality, supporting serial CO₂ gap monitoring as a practical early warning marker of deterioration. Full article

Background/Objectives: The physiological ventilation–perfusion ratio (V/Q) in the upper pulmonary field is >3 and in the lower pulmonary field it is <1 due to the effect of gravity when the body is in an upright position. Pneumonectomy leads to significant changes in ventilation and perfusion conditions. The aim of this study was to evaluate perfusion and ventilation after pneumonectomy complicated by pleural empyema, including the relationship between surgical outcomes, sex, and time from pneumonectomy. Methods: The study group included 30 patients (25 men, 5 women) who underwent pneumonectomy complicated by pleural empyema. Lung function was assessed using ventilation–perfusion scintigraphy. Twenty-one patients were assessed within 5 years after pneumonectomy and nine patients >5 years after pneumonectomy. Results: Average flow was 21.1% in the upper field, 47.8% in the middle field, and 30.35% in the lower field. The mean perfusion value was significantly higher in the lower field of the right lung than in the lower field of the left lung (33.35 vs. 28.05, p = 0.001). Average ventilation was 17.21% in the upper field, 46.73% in the middle field, and 34.28% in the lower field. The mean V/Q in the upper field was in the range of 0.81–0.87, but it reached approximately 1 (0.96–1) in the middle field and exceeded 1 (1.05–1.25) in the lower field. Conclusions: Pneumonectomy led to increased perfusion in the upper pulmonary field and increased ventilation in the lower pulmonary field compared to the literature for patients with the two lungs (the two-lung system), with a reversal of the V/Q between the upper and lower field. Full article

Background and Clinical Significance: Intermediate-high-risk pulmonary embolism is characterized by right-ventricular dysfunction and positive cardiac biomarkers in the absence of hemodynamic instability. Current guidelines recommend anticoagulation with vigilant monitoring, and reserve systemic fibrinolysis for patients who deteriorate hemodynamically. However, some patients may experience physiologic decompensation manifested by refractory hypoxemia rather than hypotension, despite preserved systemic perfusion and normal lung parenchyma. In such cases, oxygenation failure reflects the severity of perfusion impairment and incipient right-ventricular-circulatory collapse. Whether this scenario justifies systemic fibrinolysis remains uncertain. Case Presentation: We present a 75-year-old man, five days after arthroscopic meniscus repair, presenting with acute dyspnea, tachycardia, and severe respiratory failure despite normal chest radiography. Laboratory findings revealed elevated troponin-I and brain natriuretic peptide, and echocardiography demonstrated marked right-ventricular dilation. Computed tomographic pulmonary angiography confirmed extensive bilateral central emboli with preserved lung parenchyma. Despite high-flow nasal oxygen at 100% fraction of inspired oxygen, respiratory failure worsened, necessitating intubation under lung-protective settings. With catheter-directed therapy unavailable and transfer unsafe, a multidisciplinary team administered staged systemic fibrinolysis with alteplase, pausing heparin during infusion. No bleeding or surgical complications occurred. Oxygenation and right-ventricular indices improved promptly. The patient was extubated on day 2, discharged from intensive care unit on day 7, and remained asymptomatic with normal echocardiography at 3 months. Conclusions: Refractory hypoxemia in intermediate-high-risk, normotensive pulmonary embolism, particularly when parenchymal disease and ventilator confounding are excluded, may represent an early form of circulatory decompensation warranting rescue reperfusion. In the absence of catheter-directed options and with acceptable bleeding risk, staged full-dose systemic fibrinolysis can be life-saving and physiologically justified. This case supports expanding the concept of “clinical deterioration” in intermediate-risk pulmonary embolism to include isolated, unexplained respiratory failure, highlighting the need for future trials to refine individualized reperfusion thresholds. Full article

Invasive mechanical ventilation (MV) is often a lifesaving intervention in patients with traumatic brain injury (TBI) to optimize gas exchange and prevent secondary brain injury, thereby avoiding the deleterious effects of both hypoxia and hyperoxia, as well as hypocapnia and hypercapnia. However, MV in these patients represents a unique clinical challenge, as it must take into account multiple parameters, including cerebral autoregulation and autoregulatory reserves, brain compliance, cerebral dynamics such as intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral blood flow (CBF), as well as systemic hemodynamics and respiratory system mechanics. Moreover, the detrimental effects of MV on extracranial organs and systems are well established, with the lungs being the most vulnerable, particularly when non-protective ventilation strategies involving high tidal volumes (TV) and inspiratory pressures are applied. Currently, the optimal ventilation approach in patients with TBI, with or without LI, remains incompletely defined. While protective ventilation practices are recommended for a large number of critically ill patients, their application in individuals with acute brain injury (ABI) may adversely affect cerebral and systemic hemodynamics, as well as brain physiology, potentially leading to secondary damage and poor clinical outcomes. Because the consequences of TBI, such as secondary brain damage and lung complications, begin shortly after the primary event, the role of prehospital MV in these patients is crucial. However, existing data from the out-of-hospital setting are scarce. Thus, in the present review, we aim to summarize the available evidence on MV in patients with TBI, with an emphasis on the prehospital setting. Full article