scholarly journals Efficacity of Ventilator strategy in A.R.D.S (Acute Respiratory Distress Syndrome).

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Alma Cani ◽  
Fadil Gradica ◽  
Fahri Kokiçi ◽  
Loreta Agolli
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Gradual Increase ◽  
Peep Level ◽  
Arterial Oxygen Tension ◽  
Experimental Models ◽  
Arterial Oxygen ◽  
Significance Level

Background: ARDS is defined as pulmonary inflammatory process characterized by increased capillary permeability associated with acute severe hypoxemia and bilateral  infiltrates on the chest radiograph. Chlinical manifestations of ARDS is associated with a reduction of  functional residual capacity and  static compliance of the respiratory system.Recently,after experimental models and physiological studies have just established the principles to understand  the potential beneficial effects  of PEEP and reduction in mortality to 22%. The benefit of PEEP has been demonstrated in terms of preventing cyclic opening and collapsing alveoli in acute respiratory distress syndrome patients (ARDS). Aim of study: To determine  the appropriate PEEP level in-patients with ARDS. Objective: By using optimal PEEP:to realize the maximal alveolar recruitment.To avoid the decrease of oxygen delivery (DO2) as result of an unfavourable reduction in cardiac output. Material and methods:Retrospectiv study of 120 patients which only 63 of them are included in study with age 18-70 years old.(2012-2014 )  The entry criteria were clinically (severe dyspnoea, tachypnea, cyanosis); PaO2/FiO2 <200mmHG, the presence of bilateral chest infiltrates. The exclusion criteria were: aged < 18 yrs, COPD in history of diseases, heart attack; PEEP was set the level that provided the greatest improvement in oxygenation. The optimal PEEP came as a result of gradual increase of PEEP from 2-5 cmH2O every 6 hours, depended on gas analyses. The right PEEP level is the PEEP allowing the highest PaO2 value without causing hemodynamic compromise. Results: During this study we conclude that the gradual increase of PEEP improves significantly arterial oxygen tension (PaO2). Per value of PEEP 9.6-15.8, CI 95% is 145.9-191.8. The  Pearson test  with a significant correlation coefficient of level 0.995 and significance level 0.000 shows also a very important result. It was considered significant statistically the value of P≤ 0.05.  Also  the value of Chi ² of PaO2 and of PEEP, has resulted significant in 0.950 with P < 0.001. Conclusion: Mechanical ventilation using optimal PEEP increases the value of PaO2. As a matter of fact 88% of cases with PaO2 > 220 mmHg survive. The role of PEEP in clinical practice is still debated but, in selected categories of patients with a careful monitoring, it may play an important role in improving outcome.

scholarly journals Clinical characteristics and prognosis of drug-associated acute respiratory distress syndrome compared with non-drug-associated acute respiratory distress syndrome: a single-centre retrospective study in Japan

BMJ Open ◽  
2017 ◽  
Vol 7 (11) ◽  
pp. e015330 ◽  
Author(s):  
Keisuke Anan ◽  
Kazuya Ichikado ◽  
Kodai Kawamura ◽  
Takeshi Johkoh ◽  
Kiminori Fujimoto ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Arterial Oxygen Tension ◽  
Ventilator Weaning ◽  
Serum Lactate ◽  
Lung Damage ◽  
Arterial Oxygen ◽  
Serum Lactate Dehydrogenase

ObjectivesTo report the clinical features and prognosis of drug-associatedacute respiratory distress syndrome (ARDS).DesignA retrospective analysis of data collected during a prospective cohort study.SettingIntensive care unit in a teaching hospital.ParticipantsA total of 197 Japanese patients with ARDS diagnosed by the Berlin definition who were admitted to the Division of Respiratory Medicine from October 2004 to December 2015 were enrolled in the study and were classified as two groups according to their causes: a drug-associated ARDS group (n=27) and a non-drug-associated ARDS group (n=170). Primary outcome measure is 28-day mortality, and the secondaryoutcome measure is ventilator-free days.ResultsThe Acute Physiology and Chronic Health Evaluation II scores were significantly lower in the drug-associated ARDS group than in the non-drug-associated ARDS group (median (IQR): 18.0 (16.5–21.0) vs 23.0 (18.0–26.0), p<0.001), and the arterial oxygen tension/fractional inspired oxygen ratio was higher (148.0 (114.1–177.5) vs 101.0 (71.5–134.0), p=0.003). In the drug-associated ARDS group, although high-resolution CT scores indicative of the extent of fibroproliferation (301.6 (244.1–339.8) vs 208.3 (183.4–271.6), p<0.001), serum lactate dehydrogenase levels (477 (365–585) vs 322 (246–434), p=0.003) and the McCabe scores (score 1/2/3, n (%): 20 (74)/4 (15)/3 (11)vs154 (91)/7 (4)/9 (5), p=0.04) were significantly higher, ventilator weaning was earlier (p<0.001) and 28-day mortality was better (p=0.043). After adjusting for potentially confounding covariates, drug-associated ARDS group was associated with lower 28-day mortality (adjusted HR (HR) 0.275; 95% CI 0.106 to 0.711; p=0.008).ConclusionsAlthough more severe lung damage with fibroproliferation was observed in patients with drug-associated ARDS, ventilator weaning was earlier, and their prognosis was better than the others. Further well-designed prospective studies are needed.

scholarly journals Alternative and Natural Therapies for Acute Lung Injury and Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Vipul J. Patel ◽  
Sreeja Biswas Roy ◽  
Hiren J. Mehta ◽  
Myungsoo Joo ◽  
Ruxana T. Sadikot
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Experimental Models ◽  
Lung Protective Ventilation ◽  
Related Factor ◽  
Made In

Introduction. Acute respiratory distress syndrome (ARDS) is a complex clinical syndrome characterized by acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure and death. Current best practice for ARDS involves “lung-protective ventilation,” which entails low tidal volumes and limiting the plateau pressures in mechanically ventilated patients. Although considerable progress has been made in understanding the pathogenesis of ARDS, little progress has been made in the development of specific therapies to combat injury and inflammation. Areas Covered. In recent years, several natural products have been studied in experimental models and have been shown to inhibit multiple inflammatory pathways associated with acute lung injury and ARDS at a molecular level. Because of the pleiotropic effects of these agents, many of them also activate antioxidant pathways through nuclear factor erythroid-related factor 2, thereby targeting multiple pathways. Several of these agents are prescribed for treatment of inflammatory conditions in the Asian subcontinent and have shown to be relatively safe. Expert Commentary. Here we review natural remedies shown to attenuate lung injury and inflammation in experimental models. Translational human studies in patients with ARDS may facilitate treatment of this devastating disease.

Biological Impact of Transpulmonary Driving Pressure in Experimental Acute Respiratory Distress Syndrome

2015 ◽  
Vol 123 (2) ◽  
pp. 423-433 ◽  
Author(s):  
Cynthia S. Samary ◽  
Raquel S. Santos ◽  
Cíntia L. Santos ◽  
Nathane S. Felix ◽  
Maira Bentes ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Peep Level ◽  
Transpulmonary Pressure ◽  
Plateau Pressure ◽  
Driving Pressure ◽  
Ventilator Induced Lung Injury

Abstract Background: Ventilator-induced lung injury has been attributed to the interaction of several factors: tidal volume (VT), positive end-expiratory pressure (PEEP), transpulmonary driving pressure (difference between transpulmonary pressure at end-inspiration and end-expiration, ΔP,L), and respiratory system plateau pressure (Pplat,rs). Methods: Forty-eight Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, animals were randomized into combinations of VT and PEEP, yielding three different ΔP,L levels: ΔP,LLOW (VT = 6 ml/kg, PEEP = 3 cm H2O); ΔP,LMEAN (VT = 13 ml/kg, PEEP = 3 cm H2O or VT = 6 ml/kg, PEEP = 9.5 cm H2O); and ΔP,LHIGH (VT = 22 ml/kg, PEEP = 3 cm H2O or VT = 6 ml/kg, PEEP = 11 cm H2O). In other groups, at low VT, PEEP was adjusted to obtain a Pplat,rs similar to that achieved with ΔP,LMEAN and ΔP,LHIGH at high VT. Results: At ΔP,LLOW, expressions of interleukin (IL)-6, receptor for advanced glycation end products (RAGE), and amphiregulin were reduced, despite morphometric evidence of alveolar collapse. At ΔP,LHIGH (VT = 6 ml/kg and PEEP = 11 cm H2O), lungs were fully open and IL-6 and RAGE were reduced compared with ΔP,LMEAN (27.4 ± 12.9 vs. 41.6 ± 14.1 and 0.6 ± 0.2 vs. 1.4 ± 0.3, respectively), despite increased hyperinflation and amphiregulin expression. At ΔP,LMEAN (VT = 6 ml/kg and PEEP = 9.5 cm H2O), when PEEP was not high enough to keep lungs open, IL-6, RAGE, and amphiregulin expression increased compared with ΔP,LLOW (41.6 ± 14.1 vs. 9.0 ± 9.8, 1.4 ± 0.3 vs. 0.6 ± 0.2, and 6.7 ± 0.8 vs. 2.2 ± 1.0, respectively). At Pplat,rs similar to that achieved with ΔP,LMEAN and ΔP,LHIGH, higher VT and lower PEEP reduced IL-6 and RAGE expression. Conclusion: In the acute respiratory distress syndrome model used in this experiment, two strategies minimized ventilator-induced lung injury: (1) low VT and PEEP, yielding low ΔP,L and Pplat,rs; and (2) low VT associated with a PEEP level sufficient to keep the lungs open.

scholarly journals Effects of PDE3 Inhibitor Olprinone on the Respiratory Parameters, Inflammation, and Apoptosis in an Experimental Model of Acute Respiratory Distress Syndrome

2020 ◽  
Vol 21 (9) ◽  
pp. 3382
Author(s):  
Petra Kosutova ◽  
Pavol Mikolka ◽  
Sona Balentova ◽  
Marian Adamkov ◽  
Andrea Calkovska ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Arterial Oxygen Saturation ◽  
Oxygenation Index ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Respiratory Parameters ◽  
Pde3 Inhibitor

This study aimed to investigate whether a selective phosphodiesterase-3 (PDE3) inhibitor olprinone can positively influence the inflammation, apoptosis, and respiratory parameters in animals with acute respiratory distress syndrome (ARDS) model induced by repetitive saline lung lavage. Adult rabbits were divided into 3 groups: ARDS without therapy (ARDS), ARDS treated with olprinone i.v. (1 mg/kg; ARDS/PDE3), and healthy ventilated controls (Control), and were oxygen-ventilated for the following 4 h. Dynamic lung–thorax compliance (Cdyn), mean airway pressure (MAP), arterial oxygen saturation (SaO2), alveolar-arterial gradient (AAG), ratio between partial pressure of oxygen in arterial blood to a fraction of inspired oxygen (PaO2/FiO2), oxygenation index (OI), and ventilation efficiency index (VEI) were evaluated every hour. Post mortem, inflammatory and oxidative markers (interleukin (IL)-6, IL-1β, a receptor for advanced glycation end products (RAGE), IL-10, total antioxidant capacity (TAC), 3-nitrotyrosine (3NT), and malondialdehyde (MDA) and apoptosis (apoptotic index and caspase-3) were assessed in the lung tissue. Treatment with olprinone reduced the release of inflammatory mediators and markers of oxidative damage decreased apoptosis of epithelial cells and improved respiratory parameters. The results indicate a future potential of PDE3 inhibitors also in the therapy of ARDS.

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Can the Tomographic Aspect Characteristics of Patients Presenting with Acute Respiratory Distress Syndrome Predict Improvement in Oxygenation-related Response to the Prone Position?

2002 ◽  
Vol 97 (3) ◽  
pp. 599-607 ◽  
Author(s):  
Laurent Papazian ◽  
Marie-Héléne Paladini ◽  
Fabienne Bregeon ◽  
Xavier Thirion ◽  
Olivier Durieux ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Prone Position ◽  
Supine Position ◽  
Distress Syndrome ◽  
Arterial Oxygen ◽  
Computed Tomographic ◽  
Computed Tomographic Scan ◽  
A Prospective Study

Background In some patients with acute respiratory distress syndrome, the prone position is able to improve oxygenation, whereas in others it is not. It could be hypothesized that the more opacities that are present in dependent regions of the lung when the patient is in the supine position, the better the improvement in oxygenation is observed when the patients are turned prone. Therefore, we conducted a prospective study to identify computed tomographic scan aspects that could accurately predict who will respond to the prone position. Methods We included 46 patients with acute respiratory distress syndrome (31 responders and 15 nonresponders). Computed tomographic scan was performed in the 6-h period preceding prone position. Blood gas analyses were performed before and at the end of the first 6-h period of prone position. Results Arterial oxygen partial pressure/fraction of inspired oxygen increased from 117 +/- 42 (mean +/- SD) in the supine position to 200 +/- 76 mmHg in the prone position (P &lt; 0.001). There were 31 responders and 15 nonresponders. There was a vertebral predominance of the opacities (P &lt; 0.0001). However, there was no difference between responders and nonresponders. When only the amount of consolidated lung located under the heart was evaluated, there was more consolidated tissue under the heart relative to total lung area in nonresponders than in responders (P = 0.01). Conclusions There are no distinctive morphologic features in the pattern of lung disease measured by computed tomographic scanning performed with the patient in the supine position that can predict response to the prone position.

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