- Impact of "opening the lung" ventilatory strategy on burn patients with acute respiratory distress syndrome. [Journal Article]
- BBurns 2019 Jun 14
- CONCLUSIONS: It is necessary to conduct further trials to find out the effectiveness of this ventilation strategy on burns injury induced ARDS.
- Mitochondrial Division Inhibitor 1 Attenuates Mitophagy in a Rat Model of Acute Lung Injury. [Journal Article]
- BRBiomed Res Int 2019; 2019:2193706
- The regulation of intracellular mitochondria degradation is mediated by mitophagy. While studies have shown that mitophagy can lead to mitochondrial dysfunction and cell damage, the role of Mdivi-1 a…
The regulation of intracellular mitochondria degradation is mediated by mitophagy. While studies have shown that mitophagy can lead to mitochondrial dysfunction and cell damage, the role of Mdivi-1 and mitophagy remains unclear in acute lung injury (ALI) pathogenesis. In this study, we demonstrated that Mdivi-1, which is widely used as an inhibitor of mitophagy, ameliorated acute lung injury assessed by HE staining, pulmonary microvascular permeability assay, measurement of wet/dry weight (W/D) ratio, and oxygenation index (PaO2/FiO2) analysis. Then, the mitophagy related proteins were evaluated by western blot. The results indicated that LPS-induced activation of mitophagy was inhibited by Mdivi-1 treatment. In addition, we found that Mdivi-1 protected A549 cells against LPS-induced mitochondrial dysfunction. We also found that Mdivi-1 reduced pulmonary cell apoptosis in the LPS-challenged rats and protected pulmonary tissues from oxidative stress (represented by the content of superoxide dismutase, malondialdehyde and lipid peroxides in lung). Moreover, Mdivi-1 treatment ameliorated LPS-induced lung inflammatory response and cells recruitment. These findings indicate that Mdivi-1 mitigates LPS-induced apoptosis, oxidative stress, and inflammation in ALI, which may be associated with mitophagy inhibition. Thus, the inhibition of mitophagy may represent a potential therapy for treating ALI.
- Gas exchange and cardiovascular responses during breath-holding in divers: Author names and affiliations. [Journal Article]
- RPRespir Physiol Neurobiol 2019 Jun 12
- To check whether the evolution of alveolar pressures of O2 (PAO2) and CO2 (PACO2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air…
To check whether the evolution of alveolar pressures of O2 (PAO2) and CO2 (PACO2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air and in O2. We measured heart rate (fH), arterial pressure (AP), and peripheral resistances (TPR) beat-by-beat, PAO2 and PACO2 at end of each apnoea. The three phases of the cardiovascular response to apnoea were observed. In O2, TPR increase (9 ± 4 mmHg min l-1) and fH decrease (-11 ± 8 bpm) were lower than in air (15 ± 5 mmHg min l-1 and -28 ± 13 bpm, respectively). At end of maximal apnoeas in air, PAO2 and PACO2 were 50 ± 9 and 48 ± 5 mmHg, respectively; corresponding values in O2 were 653 ± 8 mmHg and 55 ± 5 mmHg. At end of phase II, PAO2 and PACO2 in air were 90 ± 13 mmHg and 42 ± 4 mmHg respectively; corresponding values in O2 were 669 ± 7 mmHg and 47 ± 6 mmHg. The PACO2 increase may trigger the AP rise in phase III.
- Ultrasound Assessment of Respiratory Workload With High-Flow Nasal Oxygen Versus Other Noninvasive Methods After Chest Surgery. [Journal Article]
- JCJ Cardiothorac Vasc Anesth 2019 May 21
- CONCLUSIONS: HFNO provides a comparable respiratory workload decrease compared with BIPAP at lower levels of pressure support and PEEP compared with SOT. Increasing BIPAP pressure support may provide higher levels of assistance but carries a risk of overdistension.
- A Comprehensive Analysis of Traumatic Rib Fractures in an Acute General Hospital in Singapore. [Journal Article]
- JEJ Emerg Trauma Shock 2019 Apr-Jun; 12(2):145-149
- CONCLUSIONS: Flail chest is associated with higher morbidity and mortality. Proactive management from a multidisciplinary team such as identification of high-risk patients in particular patients with flail chest, early admission to critical care, and protocols including multimodal pain management, respiratory support, and rehabilitation should be instituted.
- [Value of percutaneous oxygen partial pressure monitoring in evaluating the prognosis of patients with acute heart failure]. [Journal Article]
- ZWZhonghua Wei Zhong Bing Ji Jiu Yi Xue 2019; 31(5):577-581
- CONCLUSIONS: Percutaneous oxygen partial pressure monitoring can be used as a reliable indicator for prognosis evaluation of patients with AHF. Increased carbon dioxide offset and decreased 10-minute OCT suggest poor prognosis, and the prognosis of patients with AHF should be evaluated by dynamic monitoring.
- [Prognostic value of the dynamic changes in extra vascular lung water index and angiopoietin-2 in severe multiple trauma patients with acute respiratory distress syndrome]. [Journal Article]
- ZWZhonghua Wei Zhong Bing Ji Jiu Yi Xue 2019; 31(5):571-576
- CONCLUSIONS: ΔEVLWI and ΔAng-2 can be used as independent risk factors for 28-day mortality of severe multiple trauma patients with ARDS, and the predictive value of ΔEVLWI was better than Ang-2 and APACHE II. Dynamic observation of EVLWI could improve the accuracy of death forecasting for severe multiple trauma patients with ARDS.
- [Effect of high-flow nasal cannula oxygen therapy on diaphragmatic function in patients with acute exacerbation of chronic obstructive pulmonary disease: a prospective randomized controlled trial]. [Journal Article]
- ZWZhonghua Wei Zhong Bing Ji Jiu Yi Xue 2019; 31(5):551-555
- CONCLUSIONS: HFNC can effectively relieve diaphragm fatigue in patients with mild to moderate AECOPD, but it had no effect on carbon dioxide retention.
- A Scoring System with High-Resolution Computed Tomography to Predict Drug-Associated Acute Respiratory Distress Syndrome: Development and Internal Validation. [Journal Article]
- SRSci Rep 2019 Jun 13; 9(1):8601
- Drugs can cause acute respiratory distress syndrome (ARDS). However, there is no established clinical prediction rule for drug-associated ARDS (DARDS). We aimed to develop and validate a scoring syst…
Drugs can cause acute respiratory distress syndrome (ARDS). However, there is no established clinical prediction rule for drug-associated ARDS (DARDS). We aimed to develop and validate a scoring system for DARDS prediction. We analysed data collected from a prospective, single-centre, cohort study that included ARDS patients. The ARDS diagnosis was based on the American-European Consensus Conference or Berlin definition. Drug-associated acute lung injury (DALI) was defined as previous exposure to drugs which cause ALI and presence of traditional risk factors for ALI. High-resolution computed tomography (HRCT; indicating extent of lung damage with fibroproliferation), Acute Physiology and Chronic Health Evaluation (APACHE) II, and disseminated intravascular coagulation (DIC; indicating multiorgan failure) scores and PaO2/FiO2 were evaluated for their ability to predict DARDS. Twenty-nine of 229 patients had DARDS. The HRCT, APACHE II, and DIC scores and PaO2/FiO2 were assessed. The model-based predicted probability of DARDS fitted well with the observed data, and discrimination ability, assessed through bootstrap with an area under the receiver-operating curve, improved from 0.816 to 0.875 by adding the HRCT score. A simple clinical scoring system consisting of the APACHE II score, PaO2/FiO2, and DIC and HRCT scores can predict DARDS. This model may facilitate more appropriate clinical decision-making.
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- StatPearls: Noncardiogenic Pulmonary Edema [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- Noncardiogenic pulmonary edema is a disease process that results in acute hypoxia secondary to a rapid deterioration in respiratory status. The disease process has multiple etiologies, all of which r…
Noncardiogenic pulmonary edema is a disease process that results in acute hypoxia secondary to a rapid deterioration in respiratory status. The disease process has multiple etiologies, all of which require prompt recognition and intervention. Increased capillary permeability and changes in pressure gradients within the pulmonary capillaries and vasculature are mechanisms for which noncardiogenic pulmonary edema occurs. To differentiate from cardiogenic pulmonary edema, pulmonary capillary wedge pressure is not elevated and remains less than 18 mm Hg. This is important to differentiate as the management changes based on this distinction. Other findings during the initial evaluation of the patient may include a lack of acute cardiac disease or inappropriate fluid balance, flat neck veins, and the absence of peripheral edema. Chest imaging may reveal a peripheral distribution of bilateral infiltrates with no evidence of excessive pulmonary vasculature congestion or cardiomegaly. An echocardiogram may also be used to confirm a lack of acute systolic or diastolic dysfunction. These findings suggest a noncardiogenic source. Arguably the most recognized form of noncardiogenic pulmonary edema is acute respiratory distress syndrome (ARDS), which is a noncardiogenic pulmonary edema that has an acute onset secondary to an underlying inflammatory process such as sepsis, pneumonia, gastric aspiration, blood transfusion, pancreatitis, multisystem trauma or trauma to the chest wall, or drug overdose. Diagnosis of ARDS also requires bilateral infiltrates on chest x-ray with a ratio of the partial pressure of oxygen (PaO2) to the fraction of inspired oxygen (FiO2) to be less than 300 mm Hg with positive end-expiratory pressure (PEEP) of 5 cm H2O. Clinical context also necessitates no evidence of acute heart failure or hypervolemia in the setting of ARDS. The scope of noncardiogenic pulmonary edema is much broader than ARDS and includes other etiologies which include high altitude pulmonary edema, neurogenic pulmonary edema, opioid overdose, salicylate toxicity, pulmonary embolism, reexpansion pulmonary edema, reperfusion pulmonary edema, and transfusion-related acute lung injury (TRALI). Treatment is specific to the underlying etiology, and all require prompt recognition as clinical decline can be rapid and severe.