Superoxide dismutase 1-modified dental pulp stem cells alleviate high-altitude pulmonary edema by inhibiting oxidative stress through the Nrf2/HO-1 pathway.

High-altitude pulmonary edema (HAPE) is a deadly form of altitude sickness, and there is no effective treatment for HAPE. Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cell isolated from dental pulp tissues and possess various functions, such as anti-inflammatory and anti-oxidative stress. DPSCs have been used to treat a variety of diseases, but there are no studies on treating HAPE. In this study, Sprague-Dawley rats were exposed to acute low-pressure hypoxia to establish the HAPE model, and SOD1-modified DPSCs (DPSCsHiSOD1) were administered through the tail vein. Pulmonary arterial pressure, lung water content (LWC), total lung protein content of bronchoalveolar lavage fluid (BALF) and lung homogenates, oxidative stress, and inflammatory indicators were detected to evaluate the effects of DPSCsHiSOD1 on HAPE. Rat type II alveolar epithelial cells (RLE-6TN) were used to investigate the effects and mechanism of DPSCsHiSOD1 on hypoxia injury. We found that DPSCs could treat HAPE, and the effect was better than that of dexamethasone treatment. SOD1 modification could enhance the function of DPSCs in improving the structure of lung tissue, decreasing pulmonary arterial pressure and LWC, and reducing the total lung protein content of BALF and lung homogenates, through anti-oxidative stress and anti-inflammatory effects. Furthermore, we found that DPSCsHiSOD1 could protect RLE-6TN from hypoxic injury by reducing the accumulation of reactive oxygen species (ROS) and activating the Nrf2/HO-1 pathway. Our findings confirm that SOD1 modification could enhance the anti-oxidative stress ability of DPSCs through the Nrf2/HO-1 signalling pathway. DPSCs, especially DPSCsHiSOD1, could be a potential treatment for HAPE. Schematic diagram of the antioxidant stress mechanism of DPSCs in the treatment of high-altitude pulmonary edema. DPSCs can alleviate oxidative stress by releasing superoxide dismutase 1, thereby reducing ROS production and activating the Nrf2/HO-1 signalling pathway to ameliorate lung cell injury in HAPE.

Successful management of pulmonary edema secondary to accidental electrocution in a young dog.

BACKGROUND: Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes. CASE PRESENTATION: A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits. CONCLUSIONS: We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine.

Evaluation of HACOR scale as a predictor of non-invasive ventilation failure in acute cardiogenic pulmonary oedema patients: A prospective observational study.

BACKGROUND AND IMPORTANCE: Acute cardiogenic pulmonary oedema (ACPO) is a common indication for non-invasive ventilation (NIV) in the emergency department (ED). HACOR score of >5 is used to predict NIV failure. The predictive ability of HACOR may be affected by altered physiological parameters in ACPO patients due to medications or comorbidities. OBJECTIVES: To validate the HACOR scale in predicting NIV failure among acute cardiogenic pulmonary oedema (ACPO) patients. DESIGN, SETTINGS AND PARTICIPANTS: This is a prospective, observational study of consecutive ACPO patients requiring NIV admitted to the ED. OUTCOME MEASURE AND ANALYSIS: Primary outcome was the ability of the HACOR score to predict NIV failure. Clinical, physiological, and HACOR score at baseline and at 1 h, 12 h and 24 h were analysed. Other potential predictors were assessed as secondary outcomes. MAIN RESULTS: A total of 221 patients were included in the analysis. Fifty-four (24.4%) had NIV failure. Optimal HACOR score was >5 at 1 h after NIV initiation in predicting NIV failure (AUC 0.73, sensitivity 53.7%, specificity 83.2%). As part of the HACOR score, respiratory rate and heart rate were not found to be significant predictors. Other significant predictors of NIV failure in ACPO patients were acute coronary syndrome, acute kidney injury, presence of congestive heart failure as a comorbid, and the ROX index. CONCLUSIONS: The HACOR scale measured at 1 h after NIV initiation predicts NIV failure among ACPO patients with acceptable accuracy. The cut-off level > 5 could be a useful clinical decision support tool in ACPO patient. However, clinicians should consider other factors such as the acute coronary and acute kidney diagnosis at presentation, presence of underlying congestive heart failure and the ROX index when clinically deciding on timely invasive mechanical ventilation.

Continuous Positive Airway Pressure in the Treatment of Pediatric High Altitude Pulmonary Edema: A Case Study.

Treatment of high altitude pulmonary edema (HAPE) can be challenging and is further complicated in the pediatric patient in the prehospital environment. The following case presents a decompensating pediatric patient with HAPE in the prehospital aeromedical environment. It illustrates the potential benefit of continuous positive airway pressure (CPAP) as a treatment modality in the treatment of HAPE.

Reexpansion pulmonary edema after treatment of primary spontaneous pneumothorax.

A 24-year-old male patient, without further symptoms or comorbidities presented to the emergency room with acute dyspnea after heavy lifting two days before. On auscultation an attenuated vesicular breath was noticed on the right lung. In the initial chest radiograph a right-sided primary spontaneous pneumothorax with minor mediastinal shift was diagnosed. After insertion of a 12-French chest tube the patient's clinical condition deteriorated. The following chest radiograph and computed tomography of the thorax showed a reexpansion pulmonary edema in the right lung. The patient was admitted to the ICU and supportive treatment was initiated. Pulmonary reexpansion edema after drainage of a pneumothorax is a very rare complication with mortality rates reaching up to 20%. The exact pathophysiology remains unknown. Typical Symptoms include dyspnea, hypotension, and tachycardia. To minimize the risk of a pulmonary reexpansion edema, not more than 1200-1800 ml of air should be drained at once and the drainage should be stopped when the patient starts coughing.

Swimming-Induced Pulmonary Edema: Evaluation, Diagnosis, and Treatment.

ABSTRACT: Swimming-induced pulmonary edema (SIPE) is a rare but life-threatening acute illness that can occur in otherwise healthy athletes and individuals. Also known as immersion pulmonary edema, SIPE presents in swimmers, snorkelers, and SCUBA divers. It occurs in persons under heavy exertion in cold water temperatures, leading to coughing, shortness of breath, and sometimes blood-tinged sputum. Under these conditions, there is increased pulmonary vascular pressure, which may ultimately lead to pulmonary edema. This article synthesizes the latest data on the prevalence, pathophysiology, etiology, risks, short- and long-term complications, and the efficacy of supportive medical treatment interventions.

Syndromes of Concurrent Hypertension, Diastolic Dysfunction, and Pulmonary or Peripheral Edema in Cardio-Oncology: Case Studies, Literature Review, and New Classification System.

OPINION STATEMENT: Individuals who have ever been diagnosed with cancer are at increased risk for cardiovascular conditions during and after cancer treatment. Especially during cancer treatment, cardiovascular conditions can manifest in many ways, including peripheral or pulmonary edema. Edema can indicate volume overload affecting the heart even without other unequivocal evidence of apparent diastolic or systolic left ventricular dysfunction, particularly at rest. We propose a novel algorithm to streamline the diagnostic evaluation and cardiovascular classification for cancer patients with edema. We initially advise prompt evaluation with a chest X-ray and echocardiogram. We then suggest classification into one of five categories based on the timing of presentation of edema relative to cancer treatment, as well as echocardiography results and the presence or absence of hypertension or lymphatic causes of edema. This classification tool can then be utilized to guide further cardiovascular management suggestions. These concurrent syndromes presenting as edema may indicate the development or aggravation of undiagnosed diastolic dysfunction with or without hypertension, even if transiently present only while on cancer treatment.

SGLT-2 inhibitors may increase ultrafiltration in incident peritoneal dialysis patients: a case report.

BACKGROUND: Adequate fluid removal to achieve euvolemic status can be difficult in patients with incident peritoneal dialysis (PD). Limited treatments such as increased high dextrose PD solutions and icodextrin are currently available. We reported four incident PD patients whose' ultrafiltration volume was increased after sodium-glucose cotransporter-2 inhibitors. CASE PRESENTATION: The four reported cases were diabetic kidney disease stage 5 (cases 1-3) and IgA nephritis (case 4) patients whostartedt PD because of acute pulmonary edema (case 1 and 3), nausea vomiting (case 2), and hyperkalemia (case 4). They had an ultrafiltration volume of 700-1000 ml per day but hpersistentted peripheral pitting edema or pulmonary edema. Their ultrafiltration volincreased after dapagliflozin 5 mg daily, and the fluid overload symptoms ere improved. No hypotension, or hypoglycemia was found, and the urine was not increased during dapagliflozin treatment. CONCLUSIONS: SGLT-2 inhibitors may increase ultrafiltration in incident PD patients. More studies are needed to support the safety of SGLT-2 inhibitors in PD patients.

Pulmonary edema ex vacuo after drainage of pyo-pneumothorax.

This case presents a rare occurrence of re-expansion pulmonary edema following a drainage of pyo-pneumothorax in a 33-year-old patient. The diagnosis was established through a thoracic radiography, and the treatment consisted of symptomatic management, showing positive progress. Later on, the patient was diagnosed with pleural tuberculosis via GeneXpert testing and subsequently initiated on anti-bacterial therapy.This case report aims to shed light on the infrequent pulmonary edema ex vacuo as a complication of pleural drainage. It explores its causes, risk factors, diagnostic approaches, and treatment options. this study highlights the necessity of effective prevention and management strategies.

Re-expansion pulmonary edema after minimally invasive cardiac surgery in children.

Re-expansion pulmonary edema is a serious complication that can occur after minimally invasive cardiac surgery through a right mini-thoracotomy. Herein, we describe two paediatric cases where re-expansion pulmonary edema was observed after simple atrial septal defect closure through a right mini-thoracotomy. This is the first case report of re-expansion pulmonary edema after a paediatric cardiac surgery.

Pulse pressure within the first 2 days of veno-arterial extracorporeal membrane oxygenation is predictive of death prior to hospital discharge, renal dysfunction requiring dialysis and pulmonary oedema.

BACKGROUND: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) flows are titrated to achieve adequate perfusion while attempting to ideally maintain arterial pulse pressure (PP). We assessed risk in patients with low PP defined as <10 mmHg within the first 2 days of support. METHODS: Demographics, haemodynamics, echocardiographic and radiological findings were recorded retrospectively in cases conducted between 2014 and 2016. Outcomes were hospital mortality, requirement for renal replacement therapy (RRT) and severe pulmonary oedema (PO). RESULTS: Of 101 patients, 66.3% were male, mean age was 56 (range 18-71 years), mean duration of support was 6.3 days ± 4.1 days, 37.6% died prior to hospital discharge, 39.6% needed RRT and 11.9% had severe PO. Areas under the receiver operating curves of PP at 48 h for hospital mortality, RRT and severe PO were (respectively): 0.69 (95% CI 0.58-0.80, p = .001), 0.64 (95% CI 0.50-0.77, p = .044), 0.69 (95% CI 0.55-0.82, p = .009). The odds ratio for mortality, RRT, severe PO for those with low PP were (respectively) 2.8 (95% CI 1.01-7.5, p = .04), 3.1 (95% CI 1.11-8.40, p = .026), 7.6 (95% CI 2.06-27.89, p = .001). Central venous pressure, mean arterial pressure were not predictive. CONCLUSION: PP during the first 2 days of support is predictive of clinically important outcomes in patients supported with VA-ECMO.

[Negative-pressure pulmonary edema and alveolar hemorrhage are potentially life-threatening complications of upper airway obstruction]. / "Negativdruck-Lungenödem" und "alveoläre Hämorrhagie" als Komplikationen einer oberen Atemwegsobstruktion.

Negative pressure pulmonary edema and alveolar hemorrhage are potentially life-threatening complications after relief of upper airway obstruction. The laryngeal-pharyngeal obstruction results in high negative intrapleural pressures. The increased intrapleural pressures affect the integrity of the alveolo-capillary membrane due to various factors. This review describes clinical symptoms, etiologic factors, pathophysiology and treatment strategies associated with each of these factors. The aim of this review is to equip clinicians with the knowledge base necessary to identify patients at increased risk for negative pressure pulmonary edema and alveolar hemorrhage.

Endotracheal Intubation at 3,600 Meters Above Sea Level for High-Altitude Pulmonary Edema Followed by Helicopter Evacuation in Nepal.

Ranging from 64 to 8848 m above sea level, Nepal is a country rich in hilly and mountainous terrain.1 24.8% of Nepal's land area is above 3000 m, 18.9% is between 3000 and 5000 m, and 5.9% is above 5000 m.2 Hikers and trekkers are increasingly attracted to this challenging altitude and terrain, which presents risks for altitude sickness and other physical complications. Responding to medical emergencies in high-altitude areas in Nepal is highly challenging. This difficulty is often exacerbated by inclement weather, unavailability of helicopters, and poor communication regarding the location and condition of patients requiring medical attention and evacuation. High-altitude pulmonary edema (HAPE) is an illness characterized by non-cardiogenic pulmonary edema, which occurs not infrequently in individuals who rapidly ascend above 2500-3000 m in elevation,3 and which has a high mortality rate if not treated in a timely manner. Improved outcomes would be likely if skilled and equipped medical staff had better access to the sites of high-altitude expeditions in Nepal, so that life-saving interventions could be performed promptly. We report the case of a patient with HAPE who was intubated in the field at an altitude of 3600 m, and then evacuated via helicopter to a healthcare facility.

[Reexpansion edema : complication of pleural effusion drainage]. / L'image du mois. Œdème de réexpansion compliquant le drainage d'un pneumothorax.

Reexpansion pulmonary edema is a rare complication of pleural effusion drainage (liquid or gas). Its pathophysiology is not fully understood but it seems to be induced by an increase in the permeability of the alveolar-capillary membrane. The purpose of this case report is to present the clinic of reexpansion edema and also to provide practitioners with a management strategy.

Résumé : L'œdème pulmonaire de réexpansion est une complication rare du drainage d'un épanchement pleural (liquide ou gazeux). Sa physiopathologie n'est pas parfaitement comprise, mais elle semble être induite par une augmentation de la perméabilité de la membrane alvéolo-capillaire. Le but de ce rapport de cas est de présenter la clinique de l'œdème de réexpansion et également d'apporter aux praticiens une stratégie de prise en charge.

[Acute mitral insufficiency revealed by unilateral Flash Pulmonary Edema]. / L'image du mois. Insuffisance mitrale aiguë révélée par un œdème aigu du poumon unilatéral.

Flash pulmonary edema (2 % of FPE cases) is observed in 25 % of cases of acute mitral insufficiency. This clinical disorder is often mistaken for infectious pneumonitis and treated as such, with as consequence an increased mortality of these patients. The diagnosis of acute mitral insufficiency is therefore essential for the optimal management of these patients. The etiologies of mitral insufficiency can be of primary or secondary origin. Cardiac ultrasound (trans-thoracic and trans-esophageal) represent the key to the diagnosis of acute mitral insufficiency and to ensure an adapted management. It consists initially in stabilizing the patient's condition (which may be critical) via pharmacological treatments and/or mechanical support. Once stabilized, the patient can benefit from a definitive treatment of the mitral insufficiency either via valve repair (plasty) or its complete replacement.

Un oedème aigu du poumon unilatéral (2 % des cas) est retrouvé dans 25 % des cas d'insuffisance mitrale aiguë. Celui-ci est souvent confondu à tort avec une pneumopathie infectieuse et traité comme telle avec, pour conséquence, une augmentation de la mortalité. Le diagnostic d'une insuffisance mitrale aiguë est donc primordial pour une prise en charge optimale du patient. Les étiologies de celle-ci peuvent être d'origine primaire ou secondaire. L'échographie cardiaque (trans-thoracique et trans-oesophagienne) sera la clef du diagnostic d'insuffisance mitrale aiguë pour assurer une prise en charge adaptée. Celle-ci consiste, dans un premier temps, à stabiliser l'état du patient (qui peut être critique) via des traitements médicamenteux ou/et un support mécanique. Ceci permettra d'amener le patient dans des conditions optimales afin qu'il puisse bénéficier d'un traitement définitif de l'insuffisance mitrale, que ce soit via une plastie ou un remplacement complet de la valve.

A Case of Suspected Negative Pressure Pulmonary Edema after General Anesthesia.

Negative pressure pulmonary edema (NPPE) can occur rapidly after the release of an upper airway obstruction. In general anesthesia, NPPE can be caused by laryngospasm after extubation. This report describes a case in which NPPE was thought to have occurred after extubation during general anesthesia in a disabled person. The patient was a 28-yearold man, 160 cm in height and 56 kg in weight, who was scheduled for dental caries treatment under ambulatory general anesthesia due to intellectual disability. After induction of general anesthesia, nasal intubation was performed after sufficient oral suctioning to remove a large amount of serous secretion. After completion of dental treatment, pressurized extubation was performed after oral suctioning as sufficient spontaneous breathing and body movement were observed. Immediately after extubation, SpO2 dropped to 80%, subsequently recovering to 99% under oxygen administration at 5 liter/min with an oxygen mask. It dropped to approximately 85% again, however, when administration of oxygen was discontinued. Although communication with the patient was difficult, no expression of anguish or dyspnea was observed. A chest radiograph showed symmetric middle-lobe and lingular segment infiltrates, and the patient was transferred to the nearest general hospital. No obvious clinical findings other than a decrease in SpO2 were observed, suggesting NPPE as a result of airway narrowing due to secretions.

Serum Neurofilament Light Chain Levels in the Intensive Care Unit: Comparison between Severely Ill Patients with and without Coronavirus Disease 2019.

There is emerging evidence for multifarious neurological manifestations of coronavirus disease 2019 (COVID-19), but little is known regarding whether they reflect structural damage to the nervous system. Serum neurofilament light chain (sNfL) is a specific biomarker of neuronal injury. We measured sNfL concentrations of 29 critically ill COVID-19 patients, 10 critically ill non-COVID-19 patients, and 259 healthy controls. After adjusting for neurological comorbidities and age, sNfL concentrations were higher in patients with COVID-19 versus both comparator groups. Higher sNfL levels were associated with unfavorable short-term outcome, indicating that neuronal injury is common and pronounced in critically ill patients. ANN NEUROL 2021;89:610-616.

Lung ultrasound-guided management to reduce hospitalization in chronic heart failure: a systematic review and meta-analysis.

Pulmonary edema is a leading cause of hospital admissions, morbidity, and mortality in heart failure (HF) patients. A point-of-care lung ultrasound (LUS) is a useful tool to detect subclinical pulmonary edema. We performed a comprehensive literature search of multiple databases for studies that evaluated the clinical utility of LUS-guided management versus standard care for HF patients in the outpatient setting. The primary outcome of interest was HF hospitalization. The secondary outcomes were all-cause mortality, urgent visits for HF worsening, acute kidney injury (AKI), and hypokalemia rates. Pooled risk ratio (RR) and corresponding 95% confidence intervals (CIs) were calculated and combined using random-effect model meta-analysis. A total of 3 randomized controlled trials including 493 HF patients managed in the outpatient setting (251 managed with LUS plus physical examination (PE)-guided therapy vs. 242 managed with PE-guided therapy alone) were included in the final analysis. The mean follow-up period was 5 months. There was no significant difference in HF hospitalization rate between the two groups (RR 0.65; 95% CI 0.34-1.22; P = 0.18). Similarly, there was no significant difference in all-cause mortality (RR 1.39; 95% CI 0.68-2.82; P = 0.37), AKI (RR 1.27; 95% CI 0.60-2.69; P = 0.52), and hypokalemia (RR 0.72; 95% CI 0.21-2.44; P = 0.59). However, LUS-guided therapy was associated with a lower rate for urgent care visits (RR 0.32; 95% CI 0.18-0.59; P = 0.0002). Our study demonstrated that outpatient LUS-guided diuretic therapy of pulmonary congestion reduces urgent visits for worsening symptoms of HF. Further studies are needed to evaluate LUS utility in the outpatient treatment of HF.

Prediction of rehospitalization in patients with acute heart failure using point-of-care lung ultrasound.

BACKGROUND: More than 50% of patients admitted for acute heart failure are discharged with residual pulmonary congestion. Residual pulmonary congestion at discharge is associated with rehospitalization and death within 6 months after discharge. B-lines detected by lung ultrasound are the sonographic manifestation of pulmonary congestion, a major predictor of morbidity and mortality in patients with heart failure. The present study was performed to evaluate the prognostic value of B-lines at discharge for prediction of rehospitalization and death at 6 months in patients with acute heart failure. METHODS: This study involved a prospective cohort of 126 patients admitted to Ramathibodi Hospital for acute heart failure (mean age, 69 ± 15 years). B-lines and the size of the inferior vena cava were assessed within 24 h before discharge. The patients were followed up for 6 months after discharge. RESULTS: The mean number of B-lines at discharge was 9 ± 9, and the rate of rehospitalization within 6 months was significantly higher in patients with a significant number of B-lines (≥ 12) than in patients with a non-significant number of B-lines (< 12) (log rank χ2 = 7.74, P = 0.004). In the univariable analysis, the presence of ≥ 12 B-lines before discharge (hazard ratio = 2.15, 95% confidence interval = 1.27-3.63) was an independent predictor of events at 6 months. CONCLUSIONS: Residual pulmonary congestion before discharge as detected by point-of-care lung ultrasound predicts rehospitalization for heart failure at 6 months. The presence of non-significant B-lines identifies a subgroup at low risk of rehospitalization for heart failure.

Utility of non-invasive synchronized intermittent mandatory ventilation in acute cardiogenic pulmonary edema.

BACKGROUNDS: Acute cardiogenic pulmonary edema (ACPE), one of the outcomes of acute heart failure (AHF), is a common reason in a critical condition with respiratory distress. Non-invasive synchronized intermittent mandatory ventilation(nSIMV) mode, which includes inspiratory pressure in addition to positive end expiratory pressure with/without pressure support provided in the non-invasive continuous positive airway pressure plus/pressure support(nCPAP/PS) mode can be effective in hypercarbia and the associated changes in consciousness. This study aimed to demonstrate the efficacy of nSIMV in ACPE. METHODS: Patients who presented with clinical acute respiratory failure and were admitted to the critical care unit of the emergency department with the diagnosis of ACPE were included. Patients were placed on non-invasive mechanical ventilators with an oronasal mask under the nCPAP/PS and nSIMV modes. Pulse and respiratory rate, systolic and diastolic blood pressure and Glasgow Coma Scores(GCS), HACOR(heart rate, acidosis, consciousness, oxygenation and respiratory rate) scores, pH, PaCO2, PaO2/FiO2 and lactate at the time of admission and at 30 and 60 min were evaluated. RESULTS: Twenty-two patients were recruited, nCPAP/PS mode was 10 and nSIMV mode was 12. Although there was no statistically significant difference between the two groups in terms of the change in the relevant parameters from admission to 60 min, the decreases in PaCO2 and lactate levels (31.4% vs. 21.2%, p = 0.383; 68.8% vs. 47.1%, p = 0.224; respectively) and the increase in PaO2 and PaO2/FiO2 values (34% vs. 14.2%, p = 0.710 and 132.1% vs. 52.7%, p = 0.073; respectively) were higher in the nSIMV group. CONCLUSION: The nSIMV mode is as effective as the nCPAP/PS mode in the treatment of patients with ACPE. We believe that the nSIMV mode can be preferable, particularly in patients with hypercarbia who have relatively lower GCS and oxygenation.