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Background: Acute mountain sickness (AMS) is a common disease that may have a pulmonary component, as suggested by interstitial pulmonary edema quantified by the B-line score (BLS) on ultrasound (US). This subclinical pulmonary edema has been shown to increase with ascent to high altitude and AMS severity, but has not been prospectively associated with AMS incidence in a large prospective study. Materials and Methods: This prospective observational study was part of a randomized controlled trial enrolling healthy adults over four weekends ascending White Mountain, California. Subjects were assessed by lung US and the Lake Louise Questionnaire at 4110 ft (1240 m), upon ascent to 12,500 ft (3810 m), and the next morning at 12,500 ft (3810 m). Results: Three hundred five USs in total were completed on 103 participants, with 73% total incidence of AMS. The mean (±standard deviation) BLS increased from baseline (1.15 ± 1.80) to high altitude (2.56 ± 2.86), a difference of 1.37 (±2.48) ( p  = 0.04). Overall BLS was found, on average, to be higher among those diagnosed with AMS than without (2.97 vs. 2.0, p  = 0.04, 95% confidence interval [CI] -∞ to -0.04). The change in BLS (ΔBLS) from low altitude baseline was significantly associated with AMS (0.88 vs. 1.72, r 2  = 0.023, 95% CI -∞ to -0.01, p  = 0.048). Conclusions: Interstitial subclinical pulmonary edema by lung US was found to have a small but significant association with AMS.

Background: The negative pressure pulmonary edema is rare clinical situation which caused mainly by upper airway obstruction. However except upper airway obstruction, there may be other pathophysiological disorders making patients more vulnerable to pulmonary edema. Based on these disorders, upper airway obstruction is the trigger to induce negative pressure pulmonary edema., Case Presentation: This case was a 5-year-old girl with tumor on saddle area, her hormones level were abnormal preoperatively, such as cortisol, adrenocorticotrophic hormone, free T4 and total T4. During the stage of induction, negative pressure pulmonary edema took place due to mild upper airway obstruction. And the instant chest Computer tomography proved diagnosis clue. After intensive care, most lung field of this girl recovered to normal within 48 h., Conclusion: The patient with abnormal hormone levels is vulnerable to pulmonary edema, mild upper airway obstruction triggered negative pressure pulmonary. Thus pre-operation hormones supplement is as important as keeping upper airway unobstructed.

Primary graft dysfunction (PGD) is a major limitation in short- and long-term lung transplant survival. Recent work has shown that mitochondrial damage-associated molecular patterns (mtDAMPs) can promote solid organ injury, but whether they contribute to PGD severity remains unclear. We quantitated circulating plasma mitochondrial DNA (mtDNA) in 62 patients, before lung transplantation and shortly after arrival to the intensive care unit. Although all recipients released mtDNA, high levels were associated with severe PGD development. In a mouse orthotopic lung transplant model of PGD, we detected airway cell-free damaged mitochondria and mtDNA in the peripheral circulation. Pharmacologic inhibition or genetic deletion of formylated peptide receptor 1 (FPR1), a chemotaxis sensor for N-formylated peptides released by damaged mitochondria, inhibited graft injury. An analysis of intragraft neutrophil-trafficking patterns reveals that FPR1 enhances neutrophil transepithelial migration and retention within airways but does not control extravasation. Using donor lungs that express a mitochondria-targeted reporter protein, we also show that FPR1-mediated neutrophil trafficking is coupled with the engulfment of damaged mitochondria, which in turn triggers reactive oxygen species (ROS)-induced pulmonary edema. Therefore, our data demonstrate an association between mtDAMP release and PGD development and suggest that neutrophil trafficking and effector responses to damaged mitochondria are drivers of graft damage., (© 2018 The American Society of Transplantation and the American Society of Transplant Surgeons.)

Case Presentation: A 49-year-old woman with a medical history of epilepsy presented to the ED 1 h after a single, 15-min, witnessed, tonic-clonic seizure. Over the preceding 6 months, she had experienced five similar seizures of shorter duration. There were no recent changes to her phenytoin dose nor had she started any new medications. The patient had traveled to Jamaica 3 weeks before presentation, where she smoked marijuana once but otherwise had not used illicit substances nor had she used tobacco or alcohol. She states she felt well during and after the trip until this presentation. While being evaluated by the neurology service, the patient complained of sudden-onset chest pain and cough with associated hypoxemia. She denied changes in her sleep habits, she had not experienced any fevers, and she had no changes in her exercise tolerance. The patient was admitted to the general medicine floor for further workup., (Copyright © 2018 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Aims: Evaluation of the efficacy of prehospital non-invasive ventilation (NIV) in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD) and cardiogenic pulmonary edema (CPE)., Material and Methods: Consecutive patients who were prehospitally treated by Emergency Physicians using NIV were prospectively included. A step-by-step approach escalating NIV-application from continuous positive airway pressure (CPAP) to continuous positive airway pressure supplemented by pressure support (CPAP-ASB) and finally bilevel inspiratory positive airway pressure (BIPAP) was used. Patients were divided into two groups according to the prehospital NIV-treatment-time (NIV-group 1: ≤15 min, NIV-group 2: >15 min). In addition, a historic control group undergoing standard care was created. Endpoints were heart rate, peripheral oxygen saturation, breathing rate, systolic blood pressure, and a dyspnea score., Results: A total of 99 patients were analyzed (NIV-group 1: n = 41, NIV-group 2: n = 58). The control group consisted of 30 patients. The majority of NIV-patients (90%) received CPAP-ASB, while CPAP without ASB was conducted in 8% and BIPAP-ventilation in 2% of all cases. Technical application of NIV lasted 6.1 ± 3.8 min. NIV-treatment-time was as follows: NIV-group 1: 13.1 ± 3.2 min, NIV-group 2: 22.8 ± 5.9 min. Differences between baseline- and hospital admission values of all endpoints showed significantly better improvement in NIV-groups compared to the control group (p < 0.001). The stabilizing effect of NIV in terms of vital parameters was comparable between both NIV-groups, independent of the duration of treatment (n.s.)., Conclusion: Prehospital NIV-treatment should be performed in patients with COPD-exacerbation and CPE, even if the distance between emergency scene and hospital is short., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure caused by noncardiogenic pulmonary edema. Despite five decades of basic and clinical research, there is still no effective pharmacotherapy for this condition and the treatment remains primarily supportive. It is critical to study the molecular and physiologic mechanisms that cause ARDS to improve our understanding of this syndrome and reduce mortality. The goal of this review is to describe our current understanding of the pathogenesis and pathophysiology of ARDS. First, we will describe how pulmonary edema fluid accumulates in ARDS due to lung inflammation and increased alveolar endothelial and epithelial permeabilities. Next, we will review how pulmonary edema fluid is normally cleared in the uninjured lung, and describe how these pathways are disrupted in ARDS. Finally, we will explain how clinical trials and preclinical studies of novel therapeutic agents have further refined our understanding of this condition, highlighting, in particular, the study of mesenchymal stromal cells in the treatment of ARDS., Competing Interests: This work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Rationale: Diffuse alveolar hemorrhage (DAH) is a rare life-threatening condition that accompanies general anesthesia. Negative-pressure pulmonary edema (NPPE) is a rare cause of DAH., Patient Concerns: A 25-year-old male patient developed hemoptysis following remifentanil administration by bolus injection with sugammadex at the emergence from general anesthesia., Diagnosis: Chest x-ray and computed tomography showed DAH., Interventions: Conservative care was provided with 4L of oxygen via nasal prong, 20 mg of Lasix and 2500 mg of tranexamic acid., Outcomes: The patient was discharged uneventfully., Lessons: Muscle rigidity by remifentanil and the dissociated reversal of neuromuscular blockade by sugammadex was suspected as the cause of NPPE-related DAH. Therefore, the possibility NPPE-related DAH should be considered when using a bolus of remifentanil and sugammadex during emergence from general anesthesia.

Medullary hemorrhage is quite rare among brain stem hemorrhage cases, thus the clinical course remains unclear. In the medulla oblongata, respiratory centers are located and previous reports indicate that medullary lesions have possible relationship with acute respiratory distress syndrome. This kind of respiratory failure is commonly caused by neurogenic pulmonary edema (NPE), which is defined as noncardiac noninfectious acute respiratory distress syndrome with changes in intracranial condition including cerebrovascular events. However, to date, very few reports have described cases with medullary hemorrhage accompanied by NPE. We experienced 2 patients with medullary hemorrhages. A 65-year-old man presented with sudden onset of headache, whose head computed tomography showed right medullary hemorrhage. Another 76-year-old woman was transferred because of sudden limb weakness and diagnosed with left medullary hemorrhage. Digital subtraction angiography showed the presence of arteriovenous fistula in the medulla oblongata and drainer veins in the second case. Both cases were complicated by acute pulmonary edema in the early phase, suggesting the possible association of the medullary hemorrhage with NPE., (Copyright © 2018. Published by Elsevier Inc.)

Background: During the past three decades conflicting evidences have been published on the use of non-invasive ventilation (NIV) in patients with acute cardiogenic pulmonary edema (ACPE). The aim of this study is to describe the management of acute respiratory failure (ARF) due to ACPE in twelve Italian emergency departments (EDs). We evaluated prevalence, characteristics and outcomes of ACPE patients treated with oxygen therapy, continuous positive airway pressure (CPAP) or Bi-level positive airway pressure (BiPAP) on admission to the EDs., Methods: In this multicenter, prospective, observational study, consecutive adult patients with ACPE were enrolled in 12 EDs in Italy from May 2009 to December 2013. Three study groups were identified according to the initial respiratory treatment: patients receiving oxygen therapy, those treated with CPAP and those treated with BiPAP. Treatment failure was evaluated as study outcome., Results: We enrolled 1293 patients with acute cardiogenic pulmonary edema. 273 (21%) began with oxygen, 788 (61%) with CPAP and 232 (18%) with BiPAP. One out of four patient who began with oxygen was subsequently switched to NIV and initial treatment with oxygen therapy had an odds ratio for treatment failure of 3.65 (95% CI: 2.55-5.23, p < 0.001)., Conclusions: NIV seems to be the first choice for treatment of ARF due to ACPE, showing high clinical effectiveness and representing a rescue option for patients not improving with conventional oxygen therapy.

Background: A ventilator-associated events (VAEs) algorithm was developed to detect events in mechanically ventilated subjects using objective parameters, and we aimed to use objective data of fluid balance to identify pulmonary edema-associated VAEs., Methods: This single-center retrospective cohort study was conducted in a medical ICU and enrolled all mechanically ventilated patients between July 2016 and June 2017. Electronic medical records were reviewed to obtain data regarding ventilator-associated conditions (VACs), infection-related ventilator-associated complications (IVACs), possible ventilator-associated pneumonia (VAP), and traditionally defined VAP., Results: Of the 1,158 mechanically ventilated subjects, 85 (7.3%) subjects developed VAEs with a corresponding incidence rate of 7.7 events per 1,000 ventilator days. Among the 85 subjects with VAEs, 52 (61.2%) were classified as IVACs, while 23 (27.1%) had possible VAP. Notably, pulmonary edema was the main etiology (29.0%) for VAEs in the 62 subjects with non-possible VAP VAEs. Compared with those without pulmonary edema, subjects with pulmonary edema had a higher positive fluid balance 2 d before (+1,228 vs +173.5 mL, P = .005) and 1 d before (+1,622 vs +313 mL, P = .002) the diagnosis of VAE. In the multivariate logistic regression analysis (adjusted odds ratio [OR]) adjusted for potential confounders, an older age (adjusted OR 1.072, 95% CI 1.001-1.147), receiving renal replacement therapy (adjusted OR 8.906, 95% CI 1.454-54.558), and a positive cumulative difference between fluid balance 2 d and 1 d before VAE indexing (adjusted OR 1.527 per L positive, 95% CI 1.153-2.023) were independently associated with pulmonary edema in subjects with VAEs., Conclusion: These findings provide epidemiological evidence of VAEs in a medical ICU and showed that fluid balance may be used to identify pulmonary edema-associated VAEs. Further studies are warranted to validate and translate these findings into an automated surveillance system for VAEs., Competing Interests: The authors have disclosed no conflicts of interest., (Copyright © 2018 by Daedalus Enterprises.)

Objective: Renal transplantation is a risk factor for premalignant and malignant changes of the endometrium. Thus, prompt and aggressive treatment of postoperative complications remains a major issue. We report the case of an asymptomatic postmenopausal woman with a history of renal transplantation who underwent surgery for uterine serous carcinoma (USC)., Case Report: An asymptomatic 59-year-old woman who had undergone renal transplantation presented with elevated serum CA-125 levels. Cancer screening revealed uterine serous carcinoma, for which she underwent total hysterectomy and bilateral salpingo-oophorectomy. Unfortunately, the postoperative course was complicated by cardiogenic shock and decompensated heart failure. The complexities of the cardiac problems and renal transplantation required a multidisciplinary approach involving different specialists. She was successfully discharged 48 days after the surgery., Conclusion: Gynecologic cancer screening in asymptomatic postmenopausal women after renal transplantation is warranted. If postoperative complications occur in this population, a multidisciplinary approach is recommended., (Copyright © 2018. Published by Elsevier B.V.)

Neurogenic pulmonary oedema (NPO) is a rare clinical syndrome of pulmonary oedema occurring secondary to an insult of the central nervous system (CNS). The exact aetiology of this disorder is unknown. NPO can be fatal and poor awareness and identification of this entity, particularly in terms of misdiagnosis as primary pulmonary or cardiac disease, can result in suboptimal management and outcomes. We describe the presentation and management of a 68-year-old woman with an acute left lateral medullary stroke complicated by pulmonary oedema. The likely aetiology is discussed, and important learning points are highlighted., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: According to guidelines, single determination of B-type Natriuretic peptide (BNP) should be used for distinguishing between cardiac and non-cardiac acute dyspnea at the emergency room. BNP measurement is also recommended before hospital discharge in patients hospitalized for heart failure to assess prognosis and to evaluate treatment efficacy. In acute cardiogenic pulmonary edema, BNP is measured using a single BNP determination, but the temporal behavior of BNP during pulmonary edema recovery is unknown., Methods: Fifty chronic low ejection fraction (<40%) heart failure patients (age 77 ± 9 years, 17 M-33F) admitted for acute pulmonary edema were studied. Patients were grouped according to 50% dyspnea recovery time into 3 groups: ≤30 min (n = 14), 30 to 60 min (n = 19), and > 60 min (n = 17). BNP was measured at arrival and 4, 8, 12 and 24 h afterwards., Results: At arrival, BNP was elevated in all patients without significant difference among groups. In the entire population, BNP median and interquartile range value were 791 (528-1327) pg/ml, 785(559-1299) pg/ml, 1014(761-1573) pg/ml, 1049(784-1412) pg/ml, 805(497-1271) pg/ml at arrival and 4, 8, 12 and 24 h afterwards, respectively, showing higher values at 8 and 12 h. This peculiar temporal behavior of BNP was shared by all study groups. Patients with the longest edema resolution showed the highest BNP level 8 and 12 h after admission., Conclusions: In acute pulmonary edema, BNP increased up to 12 h after emergency admission regardless of dyspnea recovery time, making BNP quantitative meaning in the acute phase of pulmonary edema uncertain., (Copyright © 2018. Published by Elsevier B.V.)

Noninvasive ventilation (NIV) has assumed a central role in the treatment of selected patients with acute respiratory failure due to exacerbated chronic obstructive pulmonary disease or acute cardiogenic pulmonary edema. Recent advances in the understanding of physiologic aspects of NIV application through different interfaces and ventilator settings have led to improved patient-machine interaction, enhancing favorable NIV outcome. In recent years, the growing role of NIV in the acute care setting has led to the development of technical innovations to overcome the problems related to gas leakage and dead space, improving the quality of the devices and optimizing ventilation modes., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Acute heart failure is a common cause of admission in emergency department. Management requires rapid support when haemodynamic or respiratory parameters are altered. Identifying enabling factors and their specific treatment is an integral part of management. The most common clinical presentation is volume overload, whose treatment remains the combination of diuretics and vasodilators. In case of impaired perfusion, various inotropic supports may be considered, but also more and more circulatory assistance devices.

Background: Cardiogenic pulmonary edema (CPE) is a life-threatening emergency necessitating aggressive management. We conducted this study to test the hypothesis that a combination of N-terminal pro-b-type natriuretic peptide (NT-pro-BNP) and some relevant clinical factors may provide better predictability for CPE in heart failure (HF) patients., Methods: This retrospective study enrolled adult HF patients hospitalized during January 2011 to December 2013. After determining the independent predictors for the occurrence of CPE, a novel NT-pro BNP-based diagnostic score for predicting CPE was established., Results: A total of 269 patients (mean age, 74.5 ± 13.6 years; female, 53.9%) were enrolled, and categorized into CPE group (n = 80, 29.7%) and non-CPE group (n = 189, 70.3%). Several factors such as "Serum NT-pro-BNP level > 6980 mg/dl," "systemic blood pressure > 170 mm Hg," "heart rate > 120 bpm," "with rales in breathing sound," "with jugular vein engorgement," "with NYHA Fc III/IV," "with chronic lung disease" and "with angiotensin converting enzyme inhibitors/angiotensin receptor blocker" were found to be associated with the existence of CPE. A novel NT-pro BNP based scoring system containing these risk factors was proposed and proven excellent in predicting CPE., Conclusions: The NT-pro-BNP scoring system could predict CPE in HF patients., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The prognosis of patients with cardiogenic shock (CS) or refractory pulmonary edema because of severe aortic stenosis remains poor. The purpose of this study was to assess the outcomes of rescue percutaneous balloon aortic valvuloplasty (PBAV) in the transcatheter aortic valve implantation (TAVI) era. Patients were consecutively included between 2008 and 2016. CS was defined as ≥1 sign of systemic hypoperfusion and need of catecholamines. Refractory pulmonary edema was defined as not controlled by optimal medical treatment. A total of 40 patients, 22 men (55%), aged 79 ± 9 years, were included: 17 with CS (42.5%), 23 with refractory pulmonary edema (57.5%). After PBAV, mean transaortic gradient decreased from 47 ± 16 mm Hg to 32 ± 10 mm Hg (p < 0.001), aortic valve area increased from 0.60 ± 0.18 cm 2 to 0.88 ± 0.22 cm 2 (p < 0.0001), left ventricular ejection fraction increased from 35 ± 15 to 37 ± 14% (p = 0.02), and systolic pulmonary artery pressure decreased from 61 ± 15 to 48 ± 12 mm Hg (p = 0.002). There was no procedural death. Early death occurred in 12 patients (30%). After PBAV, 16 of the 28 survivors (57%) were bridged to surgical aortic valve replacement (SAVR; n = 7) or TAVI (n = 9), and 12 (43%) were denied definitive therapy. The 2-year estimated survival rate was 71 ± 17% after SAVR, 36 ± 19% after TAVI, and 8 ± 8% after PBAV alone. In conclusion, rescue PBAV is safe in patients with CS and high-risk aortic stenosis or refractory pulmonary edema and may improve their dismal prognosis when followed by TAVI or SAVR., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Curcumin (CUR) is a Chinese medicine monomer with antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects and mechanisms of CUR treatment on ventilator-induced lung injury (VILI) in rats., Methods: Total 50 SD rats were divided into five groups: sham, VILI, VILI+CUR-50 (CUR 50?mg/kg pretreated intraperitoneal), VILI+CUR-200 (CUR 200?mg/kg pretreated intraperitoneal) and VILI?+?DXM (5?mg/kg pretreated intraperitoneal). The morphology and ultrastructure were observed by microscope and transmission electron microscope. The wet to dry ratio, protein concentration in bronchoalveolar lavage fluid (BALF), evans blue dye (EBD) content, nuclear factor kappa B (NF-?B) activity, myeloperoxidase (MPO), malondialdehyde (MDA), xanthine oxidase (XO) and total antioxidative capacity (TAOC) levels were measured., Results: Histological studies revealed that inflammatory cells infiltration and alveolar edema were significantly severe in VILI as compared to other groups. CUR-200 and DXM treatment reversed lung injury significantly. The wet to dry ratio, protein concentration in BALF, EBD content, MPO activity, tumor necrosis factor (TNF)-? level and NF-?B activity were significantly increased in VILI group as compared to other groups. CUR-200 and DXM treatment significantly suppressed permeability and inflammation induced by ventilation. Furthermore, the significantly higher MDA content in VILI could be markedly decreased by CUR-200 and DXM treatment while the levels of XO and TAOC were markedly recovered only by CUR (200?mg/kg) treatment after VILI., Conclusion: CUR could inhibit the inflammatory response and oxidative stress during VILI, which is partly through NF-?B pathway., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Objectives: Objective measures of clinical improvement in patients with acute heart failure (AHF) are lacking. The aim of this study was to determine whether repeated lung sonography could semiquantitatively capture changes in pulmonary edema (B-lines) in patients with hypertensive AHF early in the course of treatment., Methods: We conducted a feasibility study in a cohort of adults with acute onset of dyspnea, severe hypertension in the field or at triage (systolic blood pressure ≥ 180 mm Hg), and a presumptive diagnosis of AHF. Patients underwent repeated dyspnea and lung sonographic assessments using a 10-cm visual analog scale (VAS) and an 8-zone scanning protocol. Lung sonographic assessments were performed at the time of triage, initial VAS improvement, and disposition from the emergency department. Sonographic pulmonary edema was independently scored offline in a randomized and blinded fashion by using a scoring method that accounted for both the sum of discrete B-lines and degree of B-line fusion., Results: Sonographic pulmonary edema scores decreased significantly from initial to final sonographic assessments (P < .001). The median percentage decrease among the 20 included patient encounters was 81% (interquartile range, 55%-91%). Although sonographic pulmonary edema scores correlated with VAS scores (ρ = 0.64; P < .001), the magnitude of the change in these scores did not correlate with each other (ρ = -0.04; P = .89)., Conclusions: Changes in sonographic pulmonary edema can be semiquantitatively measured by serial 8-zone lung sonography using a scoring method that accounts for B-line fusion. Sonographic pulmonary edema improves in patients with hypertensive AHF during the initial hours of treatment., (© 2017 by the American Institute of Ultrasound in Medicine.)

The use of intra-aortic balloon counter-pulsation for circulatory support in pregnant women with cardiac failure is limited to several case reports. Few publications have addressed the use of intra-aortic balloon counter-pulsation during delivery. We report a case using prophylactic intra-aortic balloon counter-pulsation during the management of a cesarean delivery in a patient with peripartum cardiomyopathy. A 28-year-old primigravid female at 37weeks of gestation was admitted with signs of worsening heart failure, and transthoracic echocardiography revealed a decreased left ventricular ejection fraction of 25%. A plan to proceed with cesarean delivery, using hemodynamic support with intra-aortic balloon counter-pulsation, was made during a multidisciplinary meeting. Shortly after initiation of intra-aortic balloon counter-pulsation, the patient's hemodynamics improved, with a decrease in heart rate and an increase in mean arterial blood pressure. After uneventful cesarean delivery of a healthy 3.2kg infant, the patient was transferred to intensive care and was extubated three hours later. Due to hemodynamic instability, intra-aortic balloon counter-pulsation support and vasopressor infusion were maintained for four postoperative days. The patient was discharged from the hospital on diuretics and beta-blocker treatment after 20days. Heart failure persisted, requiring heart transplantation 25months later. This report highlights the role of a multidisciplinary team approach in the management of delivery in an obstetric patient with peripartum cardiomyopathy., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Percutaneous treatment of chronic total occlusions (CTO) is one of the major challenges in contemporary interventional cardiology. These lesions are identified in 15% to 30% of all patients referred for coronary angiography. Percutaneous coronary intervention (PCI) of CTOs is technically challenging and requires familiarity with advanced interventional techniques as well as specialty equipment. The choice of strategy and materials is based on clinical features and coronary anatomy; the correct choice is essential to improve the success probability. PCI of CTOs is usually performed in stable coronary artery disease. We here report a case of a PCI of an anterior descending CTO grafted by a saphenous vein in an 83-year-old man admitted for acute coronary syndrome complicated by hypotensive pulmonary edema.

Rationale: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high Vt with zero positive end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to lung shear stress., Objectives: To reproduce the lung injury and edema examined in the Webb and Tierney study and to investigate the underlying mechanism thereof., Methods: Sprague-Dawley rats weighing approximately 400 g received mechanical ventilation for 60 minutes according to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H 2 O). Additional series of experiments (20 min in duration to ensure all animals survived) were studied to assess permeability (n = 4 per group), echocardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respectively)., Measurements and Main Results: The original Webb and Tierney results were replicated in terms of lung/body weight ratio (45/0 > 45/10 ≈ 30/0 ≈ 14/0; P < 0.05) and histology. In 45/0, pulmonary edema was overt and rapid, with survival less than 30 minutes. In 45/0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preload, and progressive dilation of the right ventricle. Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 45/0., Conclusions: In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately resulting in right ventricular failure and dilation. Pulmonary edema was due to increased permeability, which was augmented by a modest (approximately 40%) increase in hydrostatic pressure. The lung injury and acute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertain, but which may be due to cyclic interruption and exaggeration of pulmonary blood flow.

Objective: To investigate the risk factors for neurogenic pulmonary edema (NPE) in patients with severe hand, foot, and mouth disease (HFMD) and to provide evidence for the prevention and treatment of NPE., Methods: Several databases were searched (from inception to 2017) to identify case-control studies on risk factors for NPE among patients with severe HFMD. Data were analyzed via meta-analysis. The combined odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed-effects and random-effects models, and a sensitivity analysis and evaluation of publication bias was also performed., Results: A total of 14 studies involving 557 cases (severe HFMD with NPE) and 1450 controls (severe HFMD) were included. Results for the categorical variables were as follows: hyperglycemia (OR 10.25, 95% CI 4.82-21.76), tachycardia (OR 6.21, 95% CI 3.02-12.75), hypertension (OR 3.79, 95% CI 2.90-4.95), respiratory rhythm abnormality (OR 7.86, 95% CI 2.46-25.12), drowsiness (OR 8.11, 95% CI 4.26-15.44), vomiting (OR 8.96, 95% CI 3.83-20.96), limb tremors (OR 8.96, 95% CI 3.83-20.96), atypical rash (OR 4.27, 95% CI 2.83-6.45). No significant publication bias was found for the different factors., Conclusions: Drowsiness ranks first among risk factors for NPE in children with severe HFMD, followed by vomiting, tachycardia, hypertension, breathing rhythm changes, limb tremors, atypical rash, and hyperglycemia., (Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Aim: To establish alterations in maternal cardiac haemodynamics and function using electrocardiography and echocardiography in severe pre-eclampsia complicated by acute pulmonary oedema., Methods: An extensive literature search including any research articles, randomised control trials, observational study, case report or expert or consensus statement pertaining to severe pre-eclampsia, eclampsia, hypertensive crises of pregnancy, pulmonary oedema, maternal cardiac haemodynamics, Holter monitoring and maternal echocardiography was done. Electronic search strategies included searching the MEDLINE, EMBASE, Cochrane Library and Pubmed databases., Results: Toxic substrates from a chronically ischaemic placenta and elevated maternal cathecolamines leads to widespread elevated systemic vascular resistance, endothelial cell damage and increased left ventricular afterload all of which combine to result in left ventricular hypertrophy with impaired ventricular filling reflected as significant diastolic dysfunction, increased left ventricular end systolic and end diastolic volumes, increased left ventricular stroke work, myocardial ischaemia and resultant ventricular arrhythmias, in particular ventricular tachycardia. These factors could lead to cardiac failure in severe pre-eclampsia, either in combination or in independently of each other depending on the magnitude of the angiogenic imbalances, degree of elevated systemic vascular resistance, degree of impaired myocardial relaxation and diastolic filling anomalies, gene-environment interaction and degree of possible pre-existing or potential cardiovascular dysfunction., Conclusion: Comprehensive maternal echocardiographic and electocardiographic assessment should be incorporated in the work-up of severe pre-eclampsia to stratify these cases, to enable clinicians to choose the appropriate acute hypertensive drug therapy and plan optimal management pathways.

We describe a 36-year-old patient who was admitted to the emergency ward for acute dyspnea due to a spontaneous pneumothorax. He was successfully drained but shortly after presented a severe hypoxemia due to pulmonary oedema secondary to pulmonary re-expansion. The physiopathology behind this complication is still unknown. We will try to describe this complication and its predictive factors.

A 71-year-old male with a medical history of hypertension was admitted to emergency department with hypertensive pulmonary edema. The patient appeared anxious and diaphoretic, and physical examination revealed tachypnea, crepitant rales in the both lungs and a systolic ejection murmur at the right sternal border, radiating to the both carotid arteries. The electrocardiography showed sinus tachycardia with indications of left ventricle hypertrophy Before the aortic valve surgery, transesophageal echocardiography (TEE) was performed for detailed evaluation of the aortic valve. Two-dimensional TEE showed mild tricuspid valve regurgitation and only two of three leaflets of the tricuspid valve at a time., (© 2017, Wiley Periodicals, Inc.)

In heart failure patients, we hypothesize the occurrence of the "lung water cascade," with the various markers hierarchically ranked in a well-defined time sequence: (1) early, proximal hemodynamic event with increase in pulmonary capillary wedge pressure; (2) intermediate, direct imaging sign of pulmonary edema (easily detectable at bedside by lung ultrasound as B-lines); (3) late, distal clinical symptoms and signs such as dyspnea and pulmonary crackles. Completion of the cascade (from hemodynamic to pulmonary to clinical congestion) can require minutes (as with exercise), hours or even weeks (as with impending acute heart failure). Backward rewind of the downhill cascade can be achieved with timely pulmonary decongestion therapy, such as diuretics or dialysis, restoring a relatively dry lung. Any therapeutic intervention is more likely to succeed in the early steps of the cascade, at the imaging stage of asymptomatic pulmonary congestion, rather than downstream near to the end of the cascade, when clinical instability occurred., (© 2017, Wiley Periodicals, Inc.)

Background: To compare the application of non-invasive ventilation (NIV) versus continuous positive airway pressure (CPAP) in the treatment of patients with cardiogenic pulmonary edema (CPE) admitted to an intensive care unit (ICU)., Methods: In a prospective, randomized, controlled study performed in an ICU, patients with CPE were assigned to NIV (n=56) or CPAP (n=54). Primary outcome was intubation rate. Secondary outcomes included duration of ventilation, length of ICU and hospital stay, improvement of gas exchange, complications, ICU and hospital mortality, and 28-day mortality. The outcomes were analyzed in hypercapnic patients (PaCO 2 >45mmHg) with no underlying chronic lung disease., Results: Both devices led to similar clinical and gas exchange improvement; however, in the first 60min of treatment a higher PaO 2 /FiO 2 ratio was observed in the NIV group (205±112 in NIV vs. 150±84 in CPAP, P=.02). The rate of intubation was similar in both groups (9% in NIV vs. 9% in CPAP, P=1.0). There were no differences in duration of ventilation, ICU and length of hospital stay. There were no significant differences in ICU, hospital and 28-d mortality between groups. In the hypercapnic group, there were no differences between NIV and CPAP., Conclusions: Either NIV or CPAP are recommended in patients with CPE in the ICU. Outcomes in the hypercapnic group with no chronic lung disease were similar using NIV or CPAP., (Copyright © 2017 SEPAR. Publicado por Elsevier España, S.L.U. All rights reserved.)

Transfusion-related acute lung injury (TRALI) is defined as a new episode of acute lung injury (ALI) occurring during transfusion or within 6 hours of transfusion completion. A 66-year-old man suffering from acute myeloid leukemia developed acute respiratory distress syndrome after platelet transfusion. TRALI was diagnosed clinically, but an autopsy showed leukemic cells in diffuse pulmonary edema. Anti-human neutrophil antigen (HNA)-3a antibodies were detected in the donor serum, and the HNA-3 genotype of the patient was identified as a/a. This case was considered to represent pulmonary involvement of acute myeloid leukemia, rather than TRALI. A revision of the definition of TRALI accounting for hematological malignancies should therefore be considered.

Chronic alcohol exposure is a clinically important risk factor for the development of acute respiratory distress syndrome, the most severe form of acute lung injury (ALI). However, the mechanisms by which alcohol sensitizes the lung to development of this disease are poorly understood. We determined the role of the antifibrinolytic protein plasminogen activator inhibitor-1 (PAI-1) in alcohol enhancement of experimental endotoxin-induced ALI. Wild-type, PAI-1 -/- , and integrin β 3 -/- mice were fed ethanol-containing Lieber-DeCarli liquid or a control diet for 6 weeks, followed by systemic LPS challenge. LPS administration triggered coagulation cascade activation as evidenced by increased plasma thrombin-antithrombin levels and pulmonary fibrin deposition. Ethanol-exposed animals showed enhanced PAI-1 expression and pulmonary fibrin deposition with coincident exaggeration of pulmonary inflammatory edematous injury. PAI-1 deficiency markedly reduced pulmonary fibrin deposition and greatly reduced inflammation and injury without impacting upstream coagulation. Interestingly, pulmonary platelet accumulation was effectively abolished by PAI-1 deficiency in ethanol/LPS-challenged mice. Moreover, mice lacking integrin α IIB β 3 , the primary platelet receptor for fibrinogen, displayed a dramatic reduction in early inflammatory changes after ethanol/LPS challenge. These results indicate that the mechanism whereby alcohol exaggerates LPS-induced lung injury requires PAI-1-mediated pulmonary fibrin accumulation, and suggest a novel mechanism whereby alcohol contributes to inflammatory ALI by enhancing fibrinogen-platelet engagement.

Introduction: Pulmonary congestion is a common finding of heart failure (HF), but it remains unclear how pulmonary and heart blood volumes (V p and V h , respectively) and extravascular lung water (EVLW) change in stable HF and affect lung function., Methods: Fourteen patients with HF (age 68 ± 11 y, LVEF 33 ± 8%) and 12 control subjects (age 65 ± 9 y) were recruited. A pulmonary function test, thoracic computerized tomographic (CT) scan, and contrast perfusion scan were performed. From the thoracic scan, a histogram of CT attenuation of lung tissue was generated and skew, kurtosis, and full-width half-max (FWHM) calculated as surrogates of EVLW. Blood volumes were calculated from the transit time of the contrast through the great vessels of the heart., Results: Patients with HF had greater V p and V h (V p 0.55 ± 0.21 L vs 0.41 ± 0.13 L; V h 0.53 ± 0.33 L vs 0.40 ± 0.15 L) and EVLW (skew 3.2 ± 0.5 vs 3.7 ± 0.7; kurtosis 19.4 ± 6.6 vs 25.9 ± 9.4; FWHM 73 ± 13 HU vs 59 ± 9 HU). Spirometric measures were decreased in HF (percentage of predicted: forced vital capacity 86 ± 17% vs 104 ± 9%; forced expiratory volume in 1 second 83 ± 20% vs 105 ± 11%; maximal mid-expiratory flow 82 ± 42% vs 115 ± 43%). V p was associated with decreased expiratory flows, and EVLW was associated with decreased lung volumes., Conclusions: Congestion in stable patients with HF includes expanded V p and V h and increased EVLW associated with reductions in lung volumes and expiratory flows., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)

A 28-year-old pregnant woman presented at 28 weeks of gestation. She was diagnosed to have a left atrial myxoma 2 years earlier, but was lost to follow-up. During this pregnancy, the transthoracic echocardiography showed a 9 cm mass in the left atrium obstructing mitral valve inflow, interfering with mitral valve closure, causing severe mitral regurgitation and severe pulmonary hypertension. However, there were no clinical signs of pulmonary and systemic congestion or obstruction. Based on the clinical symptoms of the patient, the echocardiographic findings and the term of her pregnancy, the patient decided to schedule for a vaginal delivery with surgical correction after delivery. She gave birth at 32 weeks of gestation. During labour, pulmonary oedema developed but was detected early and it responded to therapy. Two weeks after delivery, a right anterior thoracotomy was performed to facilitate the removal of the left atrial myxoma and repair of the mitral valve., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Purpose: We identified risk factors for noninvasive ventilation (NIV) failure in patients with acute cardiogenic pulmonary edema (ACPE)., Materials and Methods: We conducted an observational cohort study over a 3-year period in a 28-bed emergency intensive care unit (EICU) and prospectively included all consecutive patients in whom NIV was attempted as initial ventilatory support for ACPE. The primary outcome variables were NIV failure rate and risk factors for NIV failure., Results: Among the 118 patients in the study, NIV failed for 44 (37.3%) patients. Risk factors for NIV failure were Killip class IV (odds ratio [OR], 28.56; 95% confidence interval [CI], 2.17-375.73; p=0.011), left ventricular ejection fraction (LVEF) <30% (OR, 9.54; 95% CI, 1.01-90.55; p=0.050) and B-type natriuretic peptide (BNP) ≥3350pg/mL (OR, 39.63; 95% CI, 3.92-400.79; p=0.002) at baseline, and fluid balance ≥400mL within 24h after ACPE (OR, 13.19; 95% CI, 1.18-147.70; p=0.036)., Conclusions: NIV failure occurred in 37.3% of ACPE patients in a real-world EICU. When patients had Killip class IV, a lower LVEF, a higher BNP, and a more positive fluid balance within 24h after ACPE, the risk of failure was higher. TRIAL REGISTRATION CLINICALTRIALS., Gov Identifier: NCT02653365., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The development of multiple organ failure in patients with hemorrhagic shock is significantly influenced by patient age. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator of energy homeostasis, which coordinates metabolic repair during cellular stress. We investigated whether AMPK-regulated signaling pathways are age-dependent in hemorrhage-induced lung injury and whether AMPK activation by 5-amino-4-imidazole carboxamide riboside (AICAR) affords lung protective effects. Male C57/BL6 young mice (3-5 mo), mature adult mice (9-12 mo), and young AMPKα1 knockout mice (3-5 mo) were subjected to hemorrhagic shock by blood withdrawing, followed by resuscitation with shed blood and lactated Ringer's solution. Plasma proinflammatory cytokines were similarly elevated in C57/BL6 young and mature adult mice after hemorrhagic shock. However, mature adult mice exhibited more severe lung edema and neutrophil infiltration, and higher mitochondrial damage in alveolar epithelial type II cells, than did young mice. No change in autophagy was observed. At molecular analysis, the phosphorylation of the catalytic subunit AMPKα1 was associated with nuclear translocation of peroxisome proliferator-activated receptor γ co-activator-α in young, but not mature, adult mice. Treatment with AICAR ameliorated the disruption of lung architecture in mice of both ages; however, effects in mature adult mice were different than young mice and also involved inhibition of nuclear factor-κB. In young AMPKα1 knockout mice, AICAR failed to improve hypotension and lung neutrophil infiltration. Our data demonstrate that during hemorrhagic shock, AMPK-dependent metabolic repair mechanisms are important for mitigating lung injury. However, these mechanisms are less competent with age.

Objective: A study is made of the influence of preemptive hemodynamic intervention restricting fluid administration upon the development of oleic acid-induced lung injury., Design: A randomized in vivo study in rabbits was carried out., Setting: University research laboratory., Subjects: Sixteen anesthetized, mechanically ventilated rabbits., Variables: Hemodynamic measurements obtained by transesophageal Doppler signal. Respiratory mechanics computed by a least square fitting method. Lung edema assessed by the ratio of wet weight to dry weight of the right lung. Histological examination of the left lung., Interventions: Animals were randomly assigned to either the early protective lung strategy (EPLS) (n=8) or the early protective hemodynamic strategy (EPHS) (n=8). In both groups, lung injury was induced by the intravenous infusion of oleic acid (OA) (0.133mlkg -1 h -1 for 2h). At the same time, the EPLS group received 15mlkg -1 h -1 of Ringer lactate solution, while the EPHS group received 30mlkg -1 h -1 . Measurements were obtained at baseline and 1 and 2h after starting OA infusion., Results: After 2h, the cardiac index decreased in the EPLS group (p<0.05), whereas in the EPHS group it remained unchanged. Lung compliance decreased significantly only in the EPHS group (p<0.05). Lung edema was greater in the EPHS group (p<0.05). Histological damage proved similar in both groups (p=0.4)., Conclusions: In this experimental model of early lung injury, lung edema progression was attenuated by preemptively restricting the administration of fluids., (Copyright © 2016 Elsevier España, S.L.U. y SEMICYUC. All rights reserved.)

Aim: Neurogenic pulmonary edema (NPE) is the most serious complication of subarachnoid hemorrhage (SAH). As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of NPE. We examined whether there was a relationship between vagal complex ischemia and lung immune complexes occupying the lymph node infarct in SAH., Material and Methods: Thirty-two rabbits were divided into three groups: Control (n=5), SHAM (n=5) and SAH group (n=22). SAH was created by autologous blood injection into the cisterna magna and followed-up for 3 weeks. Vasospasm index (VSI) was defined as the ratio of the lung lymph node arteries (LLNA) wall section (wall ring) surface to the lumen surface. Degenerated axon numbers of vagal nerves, neuron densities of the nodose ganglion (NG) and VSIs of LLNA were compared for all groups., Results: The mean degenerated vagal nerve axon density, neuron density of NG, and VSI of LLNA were 26±8/mm < sup > 2 < /sup > , 30±5/mm < sup > 3 < /sup > , and 0.777±0.048 in the control group; 1300±100/mm2, 720±90/mm < sup > 3 < /sup > , and 1.148±0.090 in the animals with slight vasospasm (n=12); and 7300±530/mm < sup > 2 < /sup > , 5610±810/mm3, and 1.500±0.120 in the animals with severe vasospasm (n=10), respectively., Conclusion: Degenerated vagal axon and NG neuron density may be a causative factor in the development of LLNA vasospasm induced lymph node infarct in SAH. Lung lymph node infarct may be an important factor in the prognosis of NPE.

Epidemiological studies indicate that cigarette smoking (CS) increases the risk and severity of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). The mechanism is not understood, at least in part because of lack of animal models that reproduce the key features of the CS priming process. In this study, using two strains of mice, we characterized a double-hit mouse model of ALI induced by CS priming of injury caused by lipopolysaccharide (LPS). C57BL/6 and AKR mice were preexposed to CS briefly (3 h) or subacutely (3 wk) before intratracheal instillation of LPS and ALI was assessed 18 h after LPS administration by measuring lung static compliance, lung edema, vascular permeability, inflammation, and alveolar apoptosis. We found that as little as 3 h of exposure to CS enhanced LPS-induced ALI in both strains of mice. Similar exacerbating effects were observed after 3 wk of preexposure to CS. However, there was a strain difference in susceptibility to CS priming for ALI, with a greater effect in AKR mice. The key features we observed suggest that 3 wk of CS preexposure of AKR mice is a reproducible, clinically relevant animal model that is useful for studying mechanisms and treatment of CS priming for a second-hit-induced ALI. Our data also support the concept that increased susceptibility to ALI/ARDS is an important adverse health consequence of CS exposure that needs to be taken into consideration when treating critically ill individuals.

Current guidelines for the management of patients with acute coronary syndromes (ACSs) focus on the electrocardiogram to divide patients into ST-elevation acute myocardial infarction (STEMI) or non-ST-elevation acute myocardial infarction (NSTEMI)/unstable angina (UA). Patients with STEMI in the earliest time will receive reperfusion therapy to destruct occlusive thrombus. An ST segment elevation is the 'sine qua non' for diagnosing acute total coronary occlusion causing transmural myocardial infarction. Left circumflex coronary artery (LCx) occlusion is often categorized as NSTEMI because of the absence of significant ST-elevation on the 12 lead standard electrocardiogram. An ST segment elevation is presented in fewer than 50% of patients with LCx total occlusion, such that the reperfusion therapy is delayed. We reported a 77 years old woman whom being diagnosed with NSTEMI because a 12 lead electrocardiogram showed ST segment depression in lead V2-V5. On coronary angiography, we found a total occlusion in the LCx artery as the culprit lession.