scholarly journals Combined Negative- and Positive-Pressure Ventilation for the Treatment of ARDS

2015 ◽  
Vol 2015 ◽  
pp. 1-5
Author(s):  
Konstantinos Raymondos ◽  
Jörg Ahrens ◽  
Ulrich Molitoris
Keyword(s):  
High Mortality ◽  
Negative Pressure ◽  
Pressure Support ◽  
Positive Pressure Ventilation ◽  
Standard Of Care ◽  
Positive Pressure ◽  
Current Standard ◽  
Case Presentation ◽  
Negative Pressure Ventilation

Objective. Tracheal intubation and positive-pressure ventilation as the current standard of care for the adult respiratory distress syndrome (ARDS) seem to have reached their limit in terms of a further relevant reduction of the still very high mortality.Case Presentation. A 75-year-old male patient developed ARDS after abscess drainage with deteriorating oxygenation, despite positive end-expiratory pressure (PEEP) values above 15 cm H2O. We applied external negative-pressure ventilation with a chamber respirator using −33 cm H2O at inspiration and −15 cm H2O at expiration, combined with conventional pressure support using a PEEP of about 8 cm H2O and a pressure support of 4–12 cm H2O. Alveolar infiltrates disappeared rapidly and PaO2/FiO2values surpassed 300 mmHg after the first application and 500 mmHg after the second. Negative-pressure ventilation was used for 6–18 hours/day over five days. Now, 13 years later, the patient is still alive and has a good quality of life.Conclusion. Using this or similar concepts, not only in intubated patients but also as a noninvasive approach in patients with ARDS, offers new options that may genuinely differ from the present therapeutic approaches and may, therefore, have the potential to decrease the present high mortality from ARDS.

scholarly journals Effects of Various Modes of Mechanical Ventilation in Normal Rats

2014 ◽  
Vol 120 (4) ◽  
pp. 943-950 ◽  
Author(s):  
Matteo Pecchiari ◽  
Ario Monaco ◽  
Antonia Koutsoukou ◽  
Patrizia Della Valle ◽  
Guendalina Gentile ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Negative Pressure ◽  
Positive Pressure Ventilation ◽  
Lung Mechanics ◽  
Whole Body ◽  
Positive Pressure ◽  
Negative Pressure Ventilation ◽  
Cytokine Levels

Abstract Background: Recent studies in healthy mice and rats have reported that positive pressure ventilation delivered with physiological tidal volumes at normal end-expiratory volume worsens lung mechanics and induces cytokine release, thus suggesting that detrimental effects are due to positive pressure ventilation per se. The aim of this study in healthy animals is to assess whether these adverse outcomes depend on the mode of mechanical ventilation. Methods: Rats were subjected to 4 h of spontaneous, positive pressure, and whole-body or thorax-only negative pressure ventilation (N = 8 per group). In all instances the ventilatory pattern was that of spontaneous breathing. Lung mechanics, cytokines concentration in serum and broncho–alveolar lavage fluid, lung wet-to-dry ratio, and histology were assessed. Values from eight animals euthanized shortly after anesthesia served as control. Results: No evidence of mechanical ventilation–dependent lung injury was found in terms of lung mechanics, histology, or wet-to-dry ratio. Relative to control, cytokine levels and recruitment of polymorphonuclear leucocytes increased slightly, and to the same extent with spontaneous, positive pressure, and whole-body negative pressure ventilation. Thorax-only negative pressure ventilation caused marked chest and lung distortion, reversible increase of lung elastance, and higher polymorphonuclear leucocyte count and cytokine levels. Conclusion: Both positive and negative pressure ventilation performed with tidal volumes and timing of spontaneous, quiet breathing neither elicit an inflammatory response nor cause morpho-functional alterations in normal animals, thus supporting the notion of the presence of a critical volume threshold above which acute lung injury ensues. Distortion of lung parenchyma can induce an inflammatory response, even in the absence of volotrauma.

scholarly journals Negative pressure ventilation enhances acinar perfusion in isolated rat lungs

2017 ◽  
Vol 8 (1) ◽  
pp. 204589321775359 ◽  
Author(s):  
Kal E. Watson ◽  
Gilad S. Segal ◽  
Robert L. Conhaim
Keyword(s):  
Negative Pressure ◽  
Pulmonary Circulation ◽  
Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Latex Particles ◽  
Negative Pressure Ventilation ◽  
Rat Lungs ◽  
Confocal Images ◽  
Negative Pressures ◽  
Isolated Rat

We compared acinar perfusion in isolated rat lungs ventilated using positive or negative pressures. The lungs were ventilated with air at transpulmomary pressures of 15/5 cm H2O, at 25 breaths/min, and perfused with a hetastarch solution at Ppulm art/PLA pressures of 10/0 cm H2O. We evaluated overall perfusability from perfusate flows, and from the venous concentrations of 4-µm diameter fluorescent latex particles infused into the pulmonary circulation during perfusion. We measured perfusion distribution from the trapping patterns of those particles within the lung. We infused approximately 9 million red fluorescent particles into each lung, followed 20 min later by an infusion of an equal number of green particles. In positive pressure lungs, 94.7 ± 2.4% of the infused particles remained trapped within the lungs, compared to 86.8 ± 5.6% in negative pressure lungs ( P ≤ 0.05). Perfusate flows averaged 2.5 ± 0.1 mL/min in lungs ventilated with positive pressures, compared to 5.6 ± 01 mL/min in lungs ventilated with negative pressures ( P ≤ 0.05). Particle infusions had little effect on perfusate flows. In confocal images of dried sections of each lung, red and green particles were co-localized in clusters in positive pressure lungs, suggesting that acinar vessels that lacked particles were collapsed by these pressures thereby preventing perfusion through them. Particles were more broadly and uniformly distributed in negative pressure lungs, suggesting that perfusion in these lungs was also more uniformly distributed. Our results suggest that the acinar circulation is organized as a web, and further suggest that portions of this web are collapsed by positive pressure ventilation.

Negative Pressure Ventilation and Positive Pressure Ventilation Promote Comparable Levels of Ventilator-induced Diaphragmatic Dysfunction in Rats

2013 ◽  
Vol 119 (3) ◽  
pp. 652-662 ◽  
Author(s):  
Christian S. Bruells ◽  
Ashley J. Smuder ◽  
Lucy K. Reiss ◽  
Matthew B. Hudson ◽  
William Bradley Nelson ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Negative Pressure ◽  
Positive Pressure Ventilation ◽  
Cross Sectional Area ◽  
Contractile Properties ◽  
Positive Pressure ◽  
Sectional Area ◽  
Diaphragmatic Dysfunction ◽  
Cross Sectional ◽  
Negative Pressure Ventilation

Abstract Background: Mechanical ventilation is a life-saving intervention for patients with respiratory failure. Unfortunately, a major complication associated with prolonged mechanical ventilation is ventilator-induced diaphragmatic atrophy and contractile dysfunction, termed ventilator-induced diaphragmatic dysfunction (VIDD). Emerging evidence suggests that positive pressure ventilation (PPV) promotes lung damage (ventilator-induced lung injury [VILI]), resulting in the release of signaling molecules that foster atrophic signaling in the diaphragm and the resultant VIDD. Although a recent report suggests that negative pressure ventilation (NPV) results in less VILI than PPV, it is unknown whether NPV can protect against VIDD. Therefore, the authors tested the hypothesis that compared with PPV, NPV will result in a lower level of VIDD. Methods: Adult rats were randomly assigned to one of three experimental groups (n = 8 each): (1) acutely anesthetized control (CON), (2) 12 h of PPV, and (3) 12 h of NPV. Dependent measures included indices of VILI, diaphragmatic muscle fiber cross-sectional area, diaphragm contractile properties, and the activity of key proteases in the diaphragm. Results: Our results reveal that no differences existed in the degree of VILI between PPV and NPV animals as evidenced by VILI histological scores (CON = 0.082 ± 0.001; PPV = 0.22 ± 0.04; NPV = 0.25 ± 0.02; mean ± SEM). Both PPV and NPV resulted in VIDD. Importantly, no differences existed between PPV and NPV animals in diaphragmatic fiber cross-sectional area, contractile properties, and the activation of proteases. Conclusion: These results demonstrate that NPV and PPV result in similar levels of VILI and that NPV and PPV promote comparable levels of VIDD in rats.

scholarly journals Roles of Extracellular Vesicles in High-Grade Gliomas: Tiny Particles with Outsized Influence

2019 ◽  
Vol 20 (1) ◽  
pp. 331-357 ◽  
Author(s):  
Michael W. Graner
Keyword(s):  
Extracellular Vesicles ◽  
Standard Of Care ◽  
High Grade ◽  
Biological Processes ◽  
Current Standard ◽  
Endocrine Factors ◽  
High Grade Gliomas ◽  
Endosomal System ◽  
Intercellular Communications

High-grade gliomas, particularly glioblastomas (grade IV), are devastating diseases with dismal prognoses; afflicted patients seldom live longer than 15 months, and their quality of life suffers immensely. Our current standard-of-care therapy has remained essentially unchanged for almost 15 years, with little new therapeutic progress. We desperately need a better biologic understanding of these complicated tumors in a complicated organ. One area of rejuvenated study relates to extracellular vesicles (EVs)—membrane-enclosed nano- or microsized particles that originate from the endosomal system or are shed from the plasma membrane. EVs contribute to tumor heterogeneity (including the maintenance of glioma stem cells or their differentiation), the impacts of hypoxia (angiogenesis and coagulopathies), interactions amid the tumor microenvironment (concerning the survival of astrocytes, neurons, endothelial cells, blood vessels, the blood–brain barrier, and the ensuing inflammation), and influences on the immune system (both stimulatory and suppressive). This article reviews glioma EVs and the ways that EVs manifest themselves as autocrine, paracrine, and endocrine factors in proximal and distal intra- and intercellular communications. The reader should note that there is much controversy, and indeed confusion, in the field over the exact roles for EVs in many biological processes, and we will engage some of these difficulties herein.

Simple Device for Producing Continuous Negative Pressure in Infants With IRDS

PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 128-131
Author(s):  
Eduardo Bancalari ◽  
Tilo Gerhardt ◽  
Ellen Monkus
Keyword(s):  
Intensive Care Unit ◽  
Negative Pressure ◽  
Positive Pressure Ventilation ◽  
Newborn Infants ◽  
Transpulmonary Pressure ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
School Of Medicine ◽  
Newborn Intensive Care Unit ◽  
Newborn Intensive Care

Increasing experience with the use of continuous transpulmonary pressure, either positive or negative, during the last years has clearly demonstrated the success of this mode of therapy in IRDS.1-3 Forty newborn infants with this disease have been treated with continuous negative pressure (CNP) in the Newborn Intensive Care Unit, Department of Pediatrics, University of Miami School of Medicine, using a modified incubator-respirator.* Twenty-one required only CNP, three of whom died (14%). Among the 19 who needed CNP plus intermittent positive pressure ventilation, nine died (47%). All required more than 70% oxygen to maintain a Pao2 over 50 mm Hg before using CNP.

Respiratory Effect on the Blood Volume of Pulmonary Capillaries

1988 ◽  
Vol 110 (2) ◽  
pp. 150-154 ◽  
Author(s):  
Jen-shih Lee ◽  
Timothy Fallon ◽  
Margaret Hunter ◽  
Qiang Ye ◽  
Lian-pin Lee
Keyword(s):  
Blood Volume ◽  
Positive Pressure Ventilation ◽  
Transpulmonary Pressure ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Respiratory Effect ◽  
Negative Pressure Ventilation ◽  
Aortic Blood ◽  
Pulmonary Capillaries ◽  
Ventilation Method

We measured the density variations of aortic blood from rabbits ventilated by a positive end inspiratory pressure of 6 mmHg or a negative box pressure of the same magnitude. When calculated from the density variations, the fluctuations in blood volume of the pulmonary capillaries within one cycle as induced by an intermittent positive pressure ventilation were found to be similar to the ones induced by an intermittent negative pressure ventilation. Using these volumetric fluctuations as a means to assess the transpulmonary pressure and the transmural pressure across the pulmonary capillaries, we conclude that the switching of the ventilation method did not alter the cyclic fluctuations of these pressures.

scholarly journals Clinical transplantation using negative pressure ventilation ex situ lung perfusion with extended criteria donor lungs

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Max T. Buchko ◽  
Nasim Boroumand ◽  
Jeffrey C. Cheng ◽  
Alim Hirji ◽  
Kieran Halloran ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Ex Vivo ◽  
Lung Perfusion ◽  
Ex Situ ◽  
Positive Pressure ◽  
Ex Vivo Lung Perfusion ◽  
Extended Criteria Donor ◽  
Negative Pressure Ventilation ◽  
Discharge From Hospital ◽  
End Stage

AbstractLung transplantation remains the best treatment option for end-stage lung disease; however, is limited by a shortage of donor grafts. Ex situ lung perfusion, also known as ex vivo lung perfusion, has been shown to allow for the safe evaluation and reconditioning of extended criteria donor lungs, increasing donor utilization. Negative pressure ventilation ex situ lung perfusion has been shown, preclinically, to result in less ventilator-induced lung injury than positive pressure ventilation. Here we demonstrate that, in a single-arm interventional study (ClinicalTrials.gov number NCT03293043) of 12 extended criteria donor human lungs, negative pressure ventilation ex situ lung perfusion allows for preservation and evaluation of donor lungs with all grafts and patients surviving to 30 days and recovered to discharge from hospital. This trial also demonstrates that ex situ lung perfusion is safe and feasible with no patients demonstrating primary graft dysfunction scores grade 3 at 72 h or requiring post-operative extracorporeal membrane oxygenation.

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