Search Results (207)

Background/Objectives: Patients with eosinophilic chronic obstructive pulmonary disease (COPD) often remain symptomatic despite optimized triple inhaled therapy. Dupilumab is a fully human monoclonal antibody that blocks the IL-4 receptor alpha subunit, thereby inhibiting IL-4 and IL-13 signaling. Evidence from randomized trials supports dupilumab for add-on treatment of type 2-high COPD, but data referring to short-term effectiveness in clinical practice are quite limited. Methods: We conducted an observational, compassionate-use study enrolling 13 consecutive outpatients with eosinophilic COPD (blood eosinophils ≥ 300 cells/µL) receiving add-on biologic therapy with dupilumab 300 mg every two weeks. Clinical (CAT, mMRC), functional (spirometry and body plethysmography), and inflammatory parameters (blood eosinophils/basophils, fibrinogen, FeNO) were evaluated at baseline and after four weeks of treatment. Safety was monitored after injection in a clinical setting, as well as via weekly phone follow-up. Results: Participants (84.6% male; mean age 67.08 ± 11.42 years) experienced rapid and clinically meaningful improvements at four weeks. CAT score decreased from baseline 21.40 ± 6.22 to 14.00 ± 5.58 (p < 0.001) and mMRC scale from 2.90 ± 0.73 to 1.80 ± 0.63 (p < 0.0001), respectively. Pre-bronchodilator FEV₁ increased from baseline 1.35 ± 0.65 L to 1.59 ± 0.84 L (p < 0.05), and FVC from 2.36 ± 0.92 L to 2.83 ± 1.11 L (p < 0.01). A marked lung deflation was observed: indeed, residual volume declined from baseline 4.17 ± 1.98 L to 3.47 ± 2.07 L (p < 0.05), with a concomitant reduction in specific effective airway resistance (from baseline 3.15 ± 1.77 to 2.43 ± 1.44 kPa·s; p < 0.05) associated with significant increases in mid-expiratory flow (FEF₂₅₋₇₅: from baseline 0.62 ± 0.38 to 0.86 ± 0.71 L/s; p < 0.05) and peak expiratory flow (3.80 ± 1.40 to 4.48 ± 1.79 L/s; p < 0.01). Type 2 inflammatory biomarkers changed as follows: blood eosinophil count fell from baseline 390.0 ± 43.75 to 190.0 ± 65.47 cells/µL (p < 0.001); blood basophil number decreased from baseline 37.50 ± 13.89 to 26.25 ± 13.02 cells/µL (p < 0.001); plasma fibrinogen lowered from baseline 388.4 ± 54.81 to 334.9 ± 72.36 mg/dL (p < 0.01); FeNO levels dropped from baseline 23.95 ± 18.10 to 14.00 ± 2.04 ppb (p < 0.0001). Dupilumab was well tolerated, and no treatment-related serious adverse events or discontinuations were detected. Conclusions: Within an exploratory context of daily medical activity referring to eosinophilic COPD already treated with maximal inhaled therapy, we found relevant therapeutic effects of a four-week add-on treatment with dupilumab. In particular, our patients manifested rapid improvements in symptoms, airflow limitation, and lung hyperinflation, paralleled by significant decrements of type 2 inflammatory signatures. Such encouraging results were associated with a favorable short-term safety profile. However, larger and longer studies are necessary to corroborate these preliminary findings. Full article

Background/Objectives: Flexible bronchoscopy (FB) enables airway exploration and diagnosis of various respiratory pathologies, but the sedation and instrumentation required during the procedure raise oxygen demand while reducing ventilation, which can lead to hypoxemia. Conventional oxygen therapy (COT) may not adequately prevent desaturations in high-risk groups, as patients with moderate respiratory deficiency. High-flow nasal cannula (HFNC) can deliver heated, humidified oxygen at high flow rates, generating low-level positive airway pressure, improving oxygenation, reducing dead-space, and enhancing procedure tolerance. Prior studies have shown that HFNC can improve gas exchange and reduce desaturations during bronchoscopy. However, evidence remains limited for patients with moderate respiratory deficiency, who are particularly vulnerable. Evaluating the feasibility and safety of HFNC in this population is essential to guide safe procedural practice. Methods: A retrospective observational study including patients undergoing FB with HFNC support between January and May 2025. Inclusion criteria were BMI between 18 and 30; age > 18 years old; moderate respiratory dysfunction, defined by pulse oximetry, Pulmonary Functional Tests (PFTs) and Arterial Blood Gas (ABG) analysis. Exclusion criteria were intolerance/contraindication to HFNC. Procedures were performed under basic monitoring. Primary outcome was occurrence of severe hypoxemia (SpO2 < 90%). Secondary outcomes were needed for rescue maneuvers, interruption for conversion to other ventilatory strategies, and hemodynamic instability. Results: No severe desaturations were recorded, all procedures were completed without rescue maneuvers or other ventilatory strategies, and no hypoxemia occurred. Mean duration of the procedure was 9 min. Vital parameters were maintained within the normal ranges, with a mean SpO₂ during bronchoscopy of 98%. Conclusions: HFNC enables oxygenation and ventilation without adverse events in sedations for FB in patients with moderate respiratory deficiency. Full article

Background: Durvalumab, a PD-L1 inhibitor used as consolidation therapy after chemoradiation in unresectable stage III non–small cell lung cancer (NSCLC), can induce immune-related adverse events, among which immune-mediated pneumonitis represents one of the most severe. Differentiating checkpoint inhibitor pneumonitis (CIP) from infectious pneumonia is challenging due to overlapping clinical and radiologic findings. Case presentation: We describe a 67-year-old woman with stage III lung adenocarcinoma treated with chemotherapy, radiotherapy, and durvalumab, who presented with progressive dyspnea and extensive bilateral ground-glass opacities on CT imaging. Laboratory tests revealed leukopenia and elevated inflammatory markers. Despite broad-spectrum antibiotic and antiviral therapy, her condition worsened, requiring high-flow nasal cannula oxygen therapy. Multiplex molecular testing on sputum identified human metapneumovirus (HMPV), while blood cultures and urinary antigens for Streptococcus pneumoniae and Legionella pneumophila were negative. A pulmonology consultation raised suspicion for severe durvalumab-induced pneumonitis exacerbated by viral infection. High-dose methylprednisolone (2 mg/kg/day) followed by a four-week taper led to gradual clinical and radiologic resolution. Durvalumab was permanently discontinued. Discussion: To our knowledge, this is the first reported case of HMPV-associated pneumonitis in a patient receiving durvalumab. This case highlights the potential synergistic interplay between viral infection and immune checkpoint blockade, resulting in severe lung injury. Comprehensive microbiologic evaluation, including molecular diagnostics, is essential to guide therapy and distinguish infectious from immune-mediated causes. Conclusions: Early recognition of mixed infectious and immune-mediated pneumonitis, and timely corticosteroid therapy are critical to achieving favorable outcomes and preventing irreversible pulmonary damage. Full article

Neonatal pulmonary hypertension (PH) is a major cause of illness and death in newborns. Neonatologist-performed echocardiography (NPE) is increasingly used as a bedside tool to assess heart function, shunt patterns, and pulmonary blood flow in real time, helping clinicians better understand the severity and type of PH. This narrative review summarizes current evidence on the use of NPE in diagnosing, monitoring, and treating neonatal PH, drawing on clinical studies, guidelines, and expert recommendations. NPE provides key diagnostic and therapeutic information, including evaluation of ventricular function, estimation of pulmonary pressures, and assessment of shunt direction. Advanced measures—such as tricuspid annular plane systolic excursion (TAPSE), myocardial performance index, pulmonary artery acceleration time (PAAT), and deformation imaging—improve accuracy and help guide therapies like inhaled nitric oxide, milrinone, and sildenafil. NPE is also useful in chronic conditions such as bronchopulmonary dysplasia (BPD)- and congenital diaphragmatic hernia (CDH)-associated PH. Despite its clear clinical value, NPE use remains limited by variations in training, protocols, and resource availability. Standardized curricula, accreditation, and unified reporting practices are needed to ensure safe, consistent integration of NPE into neonatal care pathways. Full article

Tricuspid atresia (TA) is a cyanotic congenital heart defect defined by agenesis of the tricuspid valve and resultant right ventricular hypoplasia, representing 1.4–2.9% of congenital heart disease. Survival depends on interatrial and interventricular shunts that permit systemic and pulmonary blood flow, with staged surgical palliation culminating in the Fontan procedure. While surgical advances have improved long-term outcomes, Fontan circulation remains a delicate physiology characterized by preload dependence, elevated pulmonary vascular resistance, chronic venous hypertension, and a prothrombotic state. These features predispose patients to arrhythmias, lymphatic complications, hepatic congestion, and progressive circulatory failure. For anesthesiologists, perioperative management of TA and Fontan patients is uniquely complex. Anesthetic considerations include meticulous preload optimization, modulation of systemic and pulmonary vascular resistance, and ventilatory strategies that minimize adverse effects on venous return. Additional challenges include the high risk of air embolism, individualized anticoagulation needs, and hemodynamic sensitivity to patient positioning. Preoperative evaluation with echocardiography and electrocardiography provides critical insight into anatomy and physiology, while intraoperative planning must emphasize goal-directed fluid management, careful agent selection, and tailored ventilation. Postoperatively, vigilant monitoring, effective pain control, and prevention of complications are essential. This review synthesizes classification systems, pathophysiology, and the evolution of surgical palliation, while emphasizing anesthetic principles for the perioperative care of patients with TA and Fontan circulation. As survival improves and the population of Fontan patients expands, a nuanced understanding of this physiology is essential for optimizing outcomes across cardiac and non-cardiac surgical settings. Full article

Background: In patients with pulmonary arterial hypertension or chronic thromboembolic pulmonary hypertension (summarized as pulmonary vascular disease; PVD), it is unclear whether the brain is protected against acute hypoxia and whether acute pulmonary vascular dilatation by sildenafil would influence cerebral and muscle tissue oxygenation whilst breathing normoxia or hypoxia. Methods: Adult patients with PVD underwent right heart catheterization, while cerebral and muscular tissue oxygenation and tissue hemoglobin index were measured using near-infrared spectroscopy along with arterial and mixed-venous blood gases. Participants underwent a four-stage protocol in which they were blinded to breathing either normoxia (FiO₂ 0.21) or normobaric hypoxia (FiO₂ 0.15), both before and after a single oral dose of sildenafil (50 mg) according to a randomized, cross-over design. Results: In 22 PVD patients (9 women, age 54 ± 14 y) under hypoxia, mean cerebral tissue oxygenation decreased by −2% (95% CI −4 to 0%, p = 0.046), muscular tissue oxygenation by −1% (95% CI −3 to 0%, p = 0.011) and mean arterial partial pressure of oxygen by −2.3 kPa (95% CI −2.7 to −1.8 kPa, p < 0.0001). Sildenafil improved the cerebral tissue hemoglobin index under hypoxia compared to hypoxia without sildenafil by 0.12 (95% CI 0.00 to 0.23, p = 0.049), but not the muscular tissue hemoglobin index. Conclusions: In PVD patients, acute exposure to normobaric hypoxia leads to a reduction in arterial oxygenation as well as cerebral and muscular tissue oxygenation. Sildenafil improves cerebral blood flow but has no effect on arterial, cerebral or muscular oxygenation. Full article

Introduction: Although the incidence of mechanical complications of myocardial infarction is decreasing, the associated mortality rate remains high. Such complications require an early diagnosis and multidisciplinary management. In most cases, surgery is the only definitive treatment, despite it being associated with high peri-operative mortality and morbidity. An intra-aortic balloon pump (IABP) or Extracorporeal Membrane Oxygenation (ECMO) may also be required for unstable patients. After the employment of mechanical assistance, ultrasound and chemical parameters are associated with successful weaning, indicating adequate cardiac function, perfusion, and oxygen delivery. Case presentation: The aim of this case report is to describe the weaning from the extracorporeal support in a case of post-myocardial-infarction ventricular septal defect (VSD) and Left ventricle (LV) apical aneurysm. The patient underwent surgery for VSD closure and aneurysm exclusion. After the emergency surgery, the patient developed a severe post-cardiotomy cardiogenic shock, which required veno-arterial femoral–femoral extracorporeal membrane oxygenation (VA-ff-ECMO), IABP, and maximal pharmacologic support. During the ICU stay, we weaned the patient from the ECMO support based on transesophageal echocardiography (TEE) imaging and pulmonary artery catheter (PAC) monitoring and quantified the shunt fraction. On the fifth post-operative day, we started the weaning trial. Hemodynamic and ultrasound monitoring showed an adequate cardiac function, and the shunt fraction calculated with both the ultrasound parameters and Fick’s law was acceptable. We removed the ECMO the day after, and the weaning was successful. Discussion: Data deriving from the Swan–Ganz catheter has been found to be important in guiding the process of weaning a patient from extracorporeal support. Nevertheless, the TEE played a pivotal role in the decision-making process and in clinical management. We reduced the ECMO blood flow following a real-time echocardiographic cardiac function assessment. Conclusions: Following the fundamental guides for both PAC monitoring and TEE imaging, we successfully removed the extracorporeal support, with a positive outcome. Full article

Subarachnoid hemorrhage (SAH), often resulting from aneurysmal rupture, remains a life-threatening cerebrovascular disorder with high morbidity and mortality. While previous research has focused primarily on cerebral damage and neurological outcomes, growing evidence suggests that SAH also causes systemic complications, including pulmonary dysfunction. The underlying mechanisms linking SAH to lung injury, however, are not fully understood. The glymphatic system, a perivascular network that facilitates the clearance of cerebrospinal fluid (CSF) and interstitial waste from the brain, plays a critical role in maintaining central nervous system (CNS) homeostasis. Aquaporin-4 (AQP4) water channels, predominantly expressed in astrocytic end feet, are essential for efficient glymphatic flow. Emerging studies have shown that SAH impairs glymphatic function by disrupting AQP4 polarity and CSF circulation, resulting in the accumulation of neurotoxic substances and neuroinflammation. Recent findings further suggest that glymphatic dysfunction may exert systemic effects beyond the CNS, contributing to a breakdown of the brain–lung axis. The release of pro-inflammatory cytokines, blood degradation products, and damage-associated molecular patterns (DAMPs) into systemic circulation can promote pulmonary endothelial injury and trigger immune responses in the lungs. This phenomenon is exacerbated by impaired clearance via the glymphatic system, amplifying systemic inflammation and increasing the risk of acute lung injury (ALI) or neurogenic pulmonary edema (NPE). This review proposes a novel perspective linking glymphatic impairment with pulmonary complications after SAH. Understanding this connection could open new therapeutic avenues—such as targeting AQP4 function, enhancing CSF circulation, or modulating the inflammatory response—to mitigate both neurological and respiratory sequelae in SAH patients. Full article

Background: There is inadequate evidence to support recommendations for the delayed clamping of umbilical cords in preterm neonates who are born non-vigorous. Objective: In a preterm bradycardic ovine model, our objective was to compare the effects of early cord clamping with ventilation (ECCV) and various time periods of delayed cord clamping with ventilation (DCCV) at 1 min (DCCV1), 2 min (DCCV2), 3 min (DCCV3), 4 min (DCCV4), and 5 min (DCCV5). The primary composite outcome was (i) incidence of achieving a combined heart rate (HR) ≥ 100 bpm and preductal saturation (SpO₂) ≥80% by 5 min, and (ii) time to attain this outcome. Secondary outcomes were to evaluate gas exchange/hemodynamics. Methods: 32 preterm lambs of 126–128-day gestational age were randomized to one of six groups: ECCV (n = 5), DCCV1 (n = 6), DCCV2 (n = 5), DCCV3 (n = 6), DCCV4 (n = 6), and DCCV5 (n = 4). Asphyxia was induced by umbilical cord occlusion to attain a HR ≤ 90 beats per minute (bpm). Results: All lambs in DCCV5 achieved a primary composite outcome by 5 min. The time taken to achieve the primary composite outcome in DCCV5 was significantly lower (p = 0.02). Partial pressure of arterial carbon dioxide (PaCO₂) was significantly lower (p = 0.0001) in DCCV5. Peak pulmonary blood flow (PBF) was significantly higher (p = 0.0001) in DCCV5 while peak carotid blood flow (CBF) was highest in the ECCV (p < 0.0001) compared to other groups. Conclusions: In a preterm ovine model of asphyxia, resuscitation with an intact umbilical cord for 5 min increased the incidence and reduced the time to achieve the primary composite outcome, while also improving gas exchange by enhancing pulmonary blood flow, compared to shorter durations of DCCV and ECCV. These findings suggest that DCCV for 5 min may offer physiological advantages in the resuscitation of non-vigorous preterm neonates, warranting further investigation in clinical settings. Full article

Background/Objectives: After pneumonectomy, the right ventricular stroke volume is pumped into pulmonary vessels whose volume has been reduced by approximately 50%. To sustain conditions for pulmonary flow, the flow reserve is increased in the remaining lung, which is conducive to the development of pulmonary hypertension symptoms. This study sought to examine pulmonary flow in one lung and the size of the right atrium (RA), right ventricle (RV) and pulmonary artery (PA) in patients who had undergone pneumonectomy and to establish the influence of time since pneumonectomy on these parameters, as well as their potential mutual dependencies. Methods: The retrospective analysis included 34 patients who had undergone pneumonectomy. Pulmonary flow was measured by means of perfusion scintigraphy. The diameters of the RA, RV and PA were evaluated based on computed tomography with contrast. Results: We observed complete or near-complete utilization of flow reserve in 38.2% (13/34) of patients, enlarged transversal and longitudinal dimensions of the RA in 17.6% (6/34) and 32.3% (11/34) of patients, respectively, and enlarged transversal and longitudinal dimension of the RV in 67.6% (23/34) and 44.1% (15/34) of patients, respectively. Dilatation of the PA was discovered in 23.5% (8/34) to 26.5% (9/34) of patients, as well as the presence of an extensive complex of radiographic features of pulmonary hypertension (PH) syndrome in 23.5% (8/34) of cases. Conclusions: Radiological features of PH were present in a significant number of patients. These features developed at varying rates but were present in all patients followed >10 years after the procedure. Full article

Background/Objectives: In a previous study, we observed significantly prolonged hepatic and pulmonary first-pass transit times (TTs) for ^99mTc-pertechnetate absorbed through the colorectal mucosa during per-rectal portal scintigraphy (PRPS). This decrease in radiotracer flow velocity was not seen when ^99mTc-pertechnetate was administered into the spleen during trans-splenic portal scintigraphy or injected intravenously in radionuclide angiocardiography. We hypothesized that ^99mTc-pertechnetate, an artificial compound, is recognized during colorectal absorption as a potentially hazardous chemical (PHC), with its hepatic and pulmonary slowdown aiding elimination. A similar sudden decrease in portal flow occurs during early metastasis of colorectal cancer (CRC), as shown by a pathological rise in the hepatic perfusion index. We aimed to study the hepatic and pulmonary vasoactive responses triggered by PHCs after they pass through the gut mucosa and evaluate the potential activation of this mechanism in early CRC metastasis. Methods: We measured transit times to determine whether hepatic and pulmonary vasoconstriction occur in response to radiotracers administered at different sites. We performed PRPS with in vivo ^99mTc-labelled RBC to evaluate the liver transit time (LTT) and right heart to liver circulation time (RHLT). Liver angioscintigraphy (LAS) was used to assess RHLT following the intravenous injection of ^99mTc-pertechnetate and ^99mTc-HDP (hydroxyethylene-diphosphate). Lower rectum transmucosal dynamic scintigraphy (LR-TMDS) was conducted to measure RHLT of ^99mTc-pertechnetate delivered into the lower rectum submucosa. LAS was performed to assess LTT for ^99mTc-HDP intravenously injected and delivered to the gut mucosa via arterial flow. Results: In healthy volunteers, PRPS showed notably increased LTT, ranging from 23.5 to 25.5 s, and RHLT (between 39.5 and 42.5 s) for in vivo ^99mTc-labelled RBC. Significantly lower RHLT values ranging from 9 to 13.5 were observed for ^99mTc-pertechnetate and ^99mTc-HDP administered intravenously during LAS, as well as for ^99mTc-pertechnetate at LR–TMDS (between 12 and 15 s). The LTT assessed at LAS for ^99mTc-HDP ranged from 22 to 27 s. Conclusions: An intense vasoconstriction occurs in the liver and lungs in response to substances recognized by the body as PHCs when they pass through the gut mucosa, aiding their elimination. Full article

Mesenchymal stromal cells (MSC) have been shown to mitigate IRI through their anti-inflammatory and immune-modulating capacities. This study aims to demonstrate the feasibility, safety, and effectiveness of hepatic administration of bone marrow-derived (BM)-MSCs in a large pig model relevant to human anatomy. After complete vascular exclusion for 45 min, 3 × 10⁶ human BM-MSCs/kg body weight were infused via the portal vein or hepatic artery. BM-MSC infusion did not cause obstruction of hepatic or pulmonary blood flow within 6 h after infusion. Cells were effectively retained in the liver, being undetectable in peripheral blood, lung, and spleen samples. Human B2M expression, as a marker for BM-MSC presence, was significantly higher for the left liver lobe in arterial infusion compared to portal infusion. In liver samples with high BM-MSC levels, we identified the prevention of up- or downregulation of some genes related to inflammation and energy metabolism that was present in non-treated control samples, indicating biological effects within 6 h of infusion. We conclude that hepatic BM-MSC infusion is feasible and safe, with the hepatic artery serving as the optimal administration route for homogenous distribution. These findings pave the way for clinical studies on MSC infusion in IRI, either in situ in liver conditions or ex situ during machine perfusion. Full article

Background/Objective: Identifying fluid-responsive patients is essential in managing hemodynamic instability. Traditional static measures like central venous pressure (CVP) are often unreliable. Prior studies suggest that cardiac ultrasound (US), particularly carotid Doppler point-of-care ultrasound (POCUS), may correlate with pulmonary artery catheter (PAC)-derived cardiac output (CO), offering a noninvasive tool to assess fluid responsiveness. We aimed to evaluate the correlation between carotid ultrasound (US) parameters and pulmonary artery catheter (PAC) derived measurements in post cardiac surgery patients. Methods: We conducted a prospective cohort study on 50 postcardiac surgery patients from 2019 to 2022 in a single cardiothoracic ICU. Carotid US and PAC CO measurements were obtained at four intervals: pre- and post-passive leg raise (fluid challenge) on ICU admission, and one hour later. Fluid responsiveness was defined as a ≥10% increase in carotid blood flow, ≥7 ms increase in corrected flow time (FTc), or ≥10% change in respiratory peak carotid systolic velocity (ΔCDPV). Pearson’s correlation and linear regression were used to assess associations between carotid US and PAC changes. Agreement in fluid responsiveness categorization (≥10% CO change) was evaluated using weighted Cohen’s kappa. Significance was set at α = 0.05. Results: No significant correlation was found between changes in carotid US parameters and the PAC cardiac index (CI) at baseline or one hour for ΔCDPV, FTc, or carotid blood flow. A moderate correlation was observed between carotid blood flow and FTc at one hour (r = 0.41, p = 0.005). Regression and sensitivity analyses showed no significant associations. Conclusions: The carotid US parameters did not correlate with PAC-derived CO after passive leg raise. Further studies are needed to validate carotid POCUS in this setting. Full article

Background: Acute aortic occlusion (AAO) is a rare but life-threatening condition which can present with a spectrum of symptoms, ranging from mild cramping pain in the lower extremities (with or without sensory loss) to more dramatic motor loss and paraplegia. Once a diagnosis has been established, the treatment remains ambiguous, especially in a resource-limited setting. Treatment ranges from direct vascular intervention to systemic or directed thrombolysis—however, there is a lack of published literature on systemic thrombolysis, and thereby, consensus guidelines are nonexistent. Additionally, systemic thrombolysis bears a risk of hemorrhagic complications; however, the risk of death due to AAO is up to 57 times greater than the risk of intracerebral hemorrhage from systemic thrombolysis. Methods: This case report explores the prompt diagnosis of an acute aortic occlusion causing bilateral acute lower extremity ischemia in a sixty-three-year-old female patient treated with systemic thrombolysis. Results: The patient received 100 mg of tPA (without a bolus dose, over a two-hour period) in the Emergency Department (similar to that which is administered for the full-dose pulmonary embolism protocol). One hour after administration, the patient had restored flow to the bilateral lower extremities verified using bedside color-flow Doppler, with a drastic improvement in her symptoms. Two days after systemic thrombolysis, a repeat CTA showed evidence of complete resolution of her aortic clot. Her condition was complicated by a brief episode of retroperitoneal bleeding (presenting with flank pain) while on a heparin drip after admission (day two), which was resolved through discontinuation of the heparin drip and a two-unit blood transfusion. Conclusion: The patient was discharged with full function of the lower extremities on day six without anticoagulation. At her 2-week follow-up appointment, she was noted to be ambulatory without any neurodeficit, with a persistently restored arterial flow to the lower extremity. The application of systemic tPA could be paramount in the treatment of AAO in the setting of ischemic limb pathology, particularly at rural hospitals and healthcare centers where urgent direct vascular intervention may not be possible. Full article

Background: This study evaluated the effects of veno-arterial (V-A) and veno-venoarterial (V-VA) ECMO in a porcine model of septic endotoxemia-induced acute pulmonary arterial hypertension (PAH). Our hypotheses were as follows: (1) V-VA ECMO lowers pulmonary vascular resistance (PVR) by delivering oxygenated blood to the pulmonary circulation, and (2) both V-A and V-VA ECMO improve perfusion to vital organs while simultaneously unloading the right ventricle (RV). Methods: Acute PAH was induced with Salmonella abortus equi lipopolysaccharide (LPS) in 34 pigs. Animals were randomized to either a control group without ECMO or to two groups receiving V-A or V-VA ECMO. Results: All animals developed PAH after one hour of LPS infusion: mean pulmonary artery pressure (PAP) increased significantly from 26 (24–30) mmHg to 40 (34–46) mmHg (p < 0.0001), and PVR increased from 314 (221–390) to 787 (549–1073) (p < 0.0001). Neither V-A nor V-VA ECMO significantly reduced PVR compared to controls. RV end-diastolic area increased in the control group [6.1 (4.3–8.6) cm vs. 8.5 (7.8–9.7) cm, p = 0.2], but not in the V-A [4.7 (3.3–7.6) cm] and V-VA [4.3 (2.5–8.3) cm] ECMO groups. Blood flow in the cranial mesenteric artery and celiac trunk did not differ significantly with or without ECMO. Conclusions: Elevating pulmonary artery oxygen tension through V-A or V-VA ECMO did not reduce PVR or PAP. However, both ECMO configurations effectively unloaded the RV and maintained perfusion to abdominal organs. Full article