scholarly journals Diaphragm neurostimulation during mechanical ventilation reduces atelectasis and transpulmonary plateau pressure, preserving lung homogeneity and PaO2/FiO2

Author(s):  
Elizabeth C. Rohrs ◽  
Thiago G. Bassi ◽  
Karl C. Fernandez ◽  
Marlena Ornowska ◽  
Michelle Nicholas ◽  
...  

Tidal volume delivered by mechanical ventilation to a sedated patient is distributed in a non-physiological pattern, causing atelectasis (underinflation) and overdistension (overinflation). Activation of the diaphragm during mechanical ventilation provides a way to reduce atelectasis and alveolar inhomogeneity, protecting the lungs from ventilator-induced lung injury while also protecting the diaphragm by preventing ventilator-induced diaphragm dysfunction. We studied the hypothesis that diaphragm contractions elicited by transvenous phrenic nerve stimulation, delivered in synchrony with volume-control ventilation, would reduce atelectasis and lung inhomogeneity in a healthy, normal-lung pig model. Twenty-five large pigs were ventilated for 50 hours with lung-protective volume-control ventilation combined with synchronous transvenous phrenic-nerve neurostimulation on every breath, or every second breath. This was compared to lung-protective ventilation alone. Lung mechanics and ventilation pressures were measured using esophageal pressure manometry and electrical impedance tomography. Alveolar homogeneity was measured using alveolar chord length of preserved lung tissue. Lung injury was measured using inflammatory cytokine concentration in bronchoalveolar lavage fluid and serum. We found that diaphragm neurostimulation on every breath preserved PaO2/FiO2 and significantly reduced the loss of end-expiratory lung volume after 50 hours of mechanical ventilation. Neurostimulation on every breath reduced plateau and driving pressures, improved both static and dynamic compliance and resulted in less alveolar inhomogeneity. These findings support that temporary transvenous diaphragm neurostimulation during volume-controlled, lung-protective ventilation may offer a potential method to provide both lung- and diaphragm-protective ventilation.

2018 ◽  
Author(s):  
Pauline K. Park ◽  
Nicole L Werner ◽  
Carl Haas

Invasive and noninvasive ventilation are important tools in the clinician’s armamentarium for managing acute respiratory failure. Although these modalities do not treat the underlying disease, they can provide the necessary oxygenation and ventilatory support until the causal pathology resolves. Care must be taken as even appropriate application can cause harm. Knowledge of pulmonary mechanics, appreciation of the basic machine settings, and an understanding of how common and advanced modes function allows the clinician to optimally tailor support to the patient while limiting iatrogenic injury. This second chapter reviews indications for mechanical ventilation, routine management, troubleshooting, and liberation from mechanical ventilation This review contains 6 figures, 7 tables and 60 references Keywords: Mechanical ventilation, lung protective ventilation, sedation, ventilator-induced lung injury, liberation from mechanical ventilation 


2004 ◽  
Vol 287 (5) ◽  
pp. L902-L910 ◽  
Author(s):  
Sharmila Choudhury ◽  
Michael R. Wilson ◽  
Michael E. Goddard ◽  
Kieran P. O'Dea ◽  
Masao Takata

Polymorphonuclear leukocytes (PMN) play an important role in ventilator-induced lung injury (VILI), but the mechanisms of pulmonary PMN recruitment, particularly early intravascular PMN sequestration during VILI, have not been elucidated. We investigated the physiological and molecular mechanisms of pulmonary PMN sequestration in an in vivo mouse model of VILI. Anesthetized C57/BL6 mice were ventilated for 1 h with high tidal volume (injurious ventilation), low tidal volume and high positive end-expiratory pressure (protective ventilation), or normal tidal volume (control ventilation). Pulmonary PMN sequestration analyzed by flow cytometry of lung cell suspensions was substantially enhanced in injurious ventilation compared with protective and control ventilation, preceding development of physiological signs of lung injury. Anesthetized, spontaneously breathing mice with continuous positive airway pressure demonstrated that raised alveolar pressure alone does not induce PMN entrapment. In vitro leukocyte deformability assay indicated stiffening of circulating leukocytes in injurious ventilation compared with control ventilation. PMN sequestration in injurious ventilation was markedly inhibited by administration of anti-L-selectin antibody, but not by anti-CD18 antibody. These results suggest that mechanical ventilatory stress initiates pulmonary PMN sequestration early in the course of VILI, and this phenomenon is associated with stretch-induced inflammatory events leading to PMN stiffening and mediated by L-selectin-dependent but CD18-independent mechanisms.


2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Chaoliang Tang ◽  
Juan Li ◽  
Shaoqing Lei ◽  
Bo Zhao ◽  
Zhetao Zhang ◽  
...  

Current evidence indicates that conventional mechanical ventilation often leads to lung inflammatory response and oxidative stress, while lung-protective ventilation (LPV) minimizes the risk of ventilator-associated lung injury (VALI). This study evaluated the effects of LPV on relief of pulmonary injury, inflammatory response, and oxidative stress among patients undergoing craniotomy. Sixty patients undergoing craniotomy received either conventional mechanical (12 mL/kg tidal volume [VT] and 0 cm H2O positive end-expiratory pressure [PEEP]; CV group) or protective lung (6 mL/kg VT and 10 cm H2O PEEP; PV group) ventilation. Hemodynamic variables, lung function indexes, and inflammatory and oxidative stress markers were assessed. The PV group exhibited greater dynamic lung compliance and lower respiratory index than the CV group during surgery (P<0.05). The PV group exhibited higher plasma interleukin- (IL-) 10 levels and lower plasma malondialdehyde and nitric oxide and bronchoalveolar lavage fluid, IL-6, IL-8, tumor necrosis factor-α, IL-10, malondialdehyde, nitric oxide, and superoxide dismutase levels (P<0.05) than the CV group. There were no significant differences in hemodynamic variables, blood loss, liquid input, urine output, or duration of mechanical ventilation between the two groups (P>0.05). Patients receiving LPV during craniotomy exhibited low perioperative inflammatory response, oxidative stress, and VALI.


2018 ◽  
Author(s):  
Pauline K. Park ◽  
Nicole L Werner ◽  
Carl Haas

Invasive and noninvasive ventilation are important tools in the clinician’s armamentarium for managing acute respiratory failure. Although these modalities do not treat the underlying disease, they can provide the necessary oxygenation and ventilatory support until the causal pathology resolves. Care must be taken as even appropriate application can cause harm. Knowledge of pulmonary mechanics, appreciation of the basic machine settings, and an understanding of how common and advanced modes function allows the clinician to optimally tailor support to the patient while limiting iatrogenic injury. This second chapter reviews indications for mechanical ventilation, routine management, troubleshooting, and liberation from mechanical ventilation This review contains 6 figures, 7 tables and 60 references Keywords: Mechanical ventilation, lung protective ventilation, sedation, ventilator-induced lung injury, liberation from mechanical ventilation 


2017 ◽  
Vol 35 (1) ◽  
pp. 37-53 ◽  
Author(s):  
Rex A. Marley ◽  
Kaycee Simon

Historically, mechanical ventilation of the lungs utilizing relatively large tidal volumes was common practice in the operating room and intensive care unit (ICU). The rationale behind this treatment strategy was to yield better patient outcomes, that is, fewer pulmonary complications, and a reduction in morbidity and mortality. As evidence-based practice has evolved, potential harmful effects of traditional, nonphysiological mechanical ventilation (ventilation with larger tidal volumes and the tolerance of high airway pressures) even in shortterm treatment have been shown to correlate with systemic inflammation and the development of ventilator-associated lung injury. Lung-protective ventilation principles using more physiological tidal volumes, avoiding high inspiratory plateau pressures, along with appropriate levels of positive end-expiratory pressure have been shown to decrease pulmonary complications and improve outcomes in patients with acute respiratory distress syndrome requiring ongoing ventilatory support in the ICU. In addition, current research is beginning to validate the benefit of providing more physiologic ventilator support in the operating room, particularly for high-risk patients undergoing major abdominal surgery, in minimizing acute lung injury. A review of lung-protective ventilation measures including benefits and potential side effects is presented. Additional treatment modalities and therapeutic considerations are offered for inclusion in optimal patient management.


2011 ◽  
Vol 39 (12) ◽  
pp. 2645-2651 ◽  
Author(s):  
Lisa M. Brown ◽  
Carolyn S. Calfee ◽  
Michael A. Matthay ◽  
Roy G. Brower ◽  
B. Taylor Thompson ◽  
...  

BMJ ◽  
2018 ◽  
pp. k3030 ◽  
Author(s):  
Brian O’Gara ◽  
Daniel Talmor

ABSTRACTPerioperative lung injury is a major source of postoperative morbidity, excess healthcare use, and avoidable mortality. Many potential inciting factors can lead to this condition, including intraoperative ventilator induced lung injury. Questions exist as to whether protective ventilation strategies used in the intensive care unit for patients with acute respiratory distress syndrome are equally beneficial for surgical patients, most of whom do not present with any pre-existing lung pathology. Studied both individually and in combination as a package of intraoperative lung protective ventilation, the use of low tidal volumes, moderate positive end expiratory pressure, and recruitment maneuvers have been shown to improve oxygenation and pulmonary physiology and to reduce postoperative pulmonary complications in at risk patient groups. Further work is needed to define the potential contributions of alternative ventilator strategies, limiting excessive intraoperative oxygen supplementation, use of non-invasive techniques in the postoperative period, and personalized mechanical ventilation. Although the weight of evidence strongly suggests a role for lung protective ventilation in moderate risk patient groups, definitive evidence of its benefit for the general surgical population does not exist. However, given the shift in understanding of what is needed for adequate oxygenation and ventilation under anesthesia, the largely historical arguments against the use of intraoperative lung protective ventilation may soon be outdated, on the basis of its expanding track record of safety and efficacy in multiple settings.


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