No abstract available.
Ventilator-Induced Lung Injury* ; Ventilators, Mechanical*

For patients receiving mechanical ventilation, mechanical ventilation is also an injury factor at the same time of treatment, which can lead to or aggravate lung injury, that is, ventilator-induced lung injury (VILI). The typical feature of VILI is that the mechanical stress is transmitted to cells through the pathway, leading to uncontrollable inflammatory cascade reaction, which causes the activation of inflammatory cells in the lung and the release of a large number of cytokines and inflammatory mediators. Among them, innate immunity is also involved in the occurrence and development of VILI. A large number of studies have shown that damaged lung tissue in VILI can regulate inflammatory response by releasing a large number of damage associated molecular pattern (DAMP). Pattern recognition receptor (PRR) participates in the activation of immune response by combining with DAMP, and releases a large number of inflammatory mediators to promote the occurrence and development of VILI. Recent studies have shown that inhibition of DAMP/PRR signaling pathway can play a protective role in VILI. Therefore, this article will mainly discuss the potential role of blocking DAMP/PRR signal pathway in VILI, and provide new ideas for the treatment of VILI.
Humans ; Respiration, Artificial ; Respiration ; Immunity, Innate ; Ventilator-Induced Lung Injury ; Inflammation ; Inflammation Mediators ; Lung

This paper compares and describes the tidal volume (Vt) used in mechanically ventilated dogs under a range of clinical conditions. Twenty-eight dogs requiring mechanical ventilation (MV) were classified into 3 groups: healthy dogs mechanically ventilated during surgery (group I, n = 10), dogs requiring MV due to extra-pulmonary reasons (group II, n = 7), and dogs that required MV due to pulmonary pathologies (group III, n = 11). The median Vt used in each group was 16 mL/kg (interquartile range [IQR], 15.14–21) for group I, 12.59 mL/kg (IQR, 9–14.25) for group II, and 12.59 mL/kg (IQR, 10.15–14.96) for group III. The Vt used was significantly lower in group III than in group I (p = 0.016). The thoraco-pulmonary compliance was significantly higher in group I than in groups II and III (p = 0.011 and p = 0.006, respectively). The median driving pressure was similar among the groups with a median of 9, 11, and 10 cmH2O in groups I, II, and III, respectively (p = 0.260). Critically-ill dogs requiring MV due to the primary pulmonary pathology received a significantly lower Vt than healthy dogs but with a range of values that were markedly higher than those recommended by human guidelines.
Animals ; Compliance ; Dogs ; Humans ; Pathology ; Respiration, Artificial ; Tidal Volume ; Ventilator-Induced Lung Injury

Despite the advanced technologies of intensive care, massive hemoptysis can still cause death in a small subset of patients. Extracorporeal membrane oxygenation (ECMO) is expected to provide adequate gas exchange, to reduce ventilator-induced lung injuries, and to eventually improve outcomes in these patients. Also, the instability of vital signs due to hemoptysis makes it impossible to perform immediate interventional procedures such as embolization and resectional surgery. In these cases, ECMO may be instituted as a bridge therapy. Herein, we describe the detailed course of our case, with the hopes of helping physicians to decide when to initiate ECMO in patients with massive hemoptysis.
Anoxia ; Extracorporeal Membrane Oxygenation ; Hemoptysis ; Humans ; Critical Care ; Ventilator-Induced Lung Injury ; Vital Signs

Lung-protective ventilation (such as low tidal volume and application of positive end-expiratory pressure) is beneficial for patients with acute lung injury or acute respiratory distress syndrome (ARDS) and has become the standard treatment in intensive care unit (ICU). However, some experts now question whether the protective ventilation strategy for ARDS patients in the ICU is equally beneficial for patients after surgery, especially for most patients without any pre-existing lung lesions. This review will discuss preoperative, intraoperative, and postoperative lung protection strategies to reduce the risk of complications associated with anesthesia.
Humans ; Positive-Pressure Respiration ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Tidal Volume ; Ventilator-Induced Lung Injury

ObjectiveMechanical ventilation (MV) has long been used as a life-sustaining approach for several decades. However, researchers realized that MV not only brings benefits to patients but also cause lung injury if used improperly, which is termed as ventilator-induced lung injury (VILI). This review aimed to discuss the pathogenesis of VILI and the underlying molecular mechanisms.

Data SourcesThis review was based on articles in the PubMed database up to December 2017 using the following keywords: "ventilator-induced lung injury", "pathogenesis", "mechanism", and "biotrauma".

Study SelectionOriginal articles and reviews pertaining to mechanisms of VILI were included and reviewed.

ResultsThe pathogenesis of VILI was defined gradually, from traditional pathological mechanisms (barotrauma, volutrauma, and atelectrauma) to biotrauma. High airway pressure and transpulmonary pressure or cyclic opening and collapse of alveoli were thought to be the mechanisms of barotraumas, volutrauma, and atelectrauma. In the past two decades, accumulating evidence have addressed the importance of biotrauma during VILI, the molecular mechanism underlying biotrauma included but not limited to proinflammatory cytokines release, reactive oxygen species production, complement activation as well as mechanotransduction.

ConclusionsBarotrauma, volutrauma, atelectrauma, and biotrauma contribute to VILI, and the molecular mechanisms are being clarified gradually. More studies are warranted to figure out how to minimize lung injury induced by MV.

Animals ; Barotrauma ; metabolism ; Humans ; Reactive Oxygen Species ; metabolism ; Ventilator-Induced Lung Injury ; metabolism ; Wounds and Injuries ; metabolism

BACKGROUND: Since the late 1960s, mechanical ventilation has been accomplished primarily using volume controlled ventilation(VCV). While VCV allows a set tidal volume to be guaranteed, VCV could bring about excessive airway pressures that may be lead to barotrauma in the patients with acute lung injury. With the increment of knowledge related to ventilator-induced lung injury, pressure controlled ventilation(PCV) has been frequenfly applied to these patients. But, PCV has a disadvantage of variable tidal volume delivery as pulinonary impedance changes. Since the concept of combining the positive attributes of VCV and PCV(dual control ventilation, DCV) was described firstly in 1992, a few DCV modes were introduced. Pressure-regulated volume control(PRVC) mode, a kind of DCV, is pressure-limited, time-cycled ventilation that uses tidal volume as a feedback control for continuously adjusting the pressure limit. However, no clinical studies were published on the efficacy of PRVC until now. This investigation studied the efficacy of PRVC in the patients with unstable respiratory mechanics. METHODS: The subjects were 8 mechanically ventilated patients(M: F= 6 : 2, 56+/-26 years) who showed unstable respiratory mechanics, which was defined by the coefficients of variation of peak inspiratory pressure for 15 minutes greater than 10% under VCV, or the coefficients of variation of tidal volume greater than 10% under PCV. The study was consisited of 3 modes application with VCV, PCV and PRVC for 15 minutes by random order. To obtain same tidal volume, inspiratory pressure setting was adjusted in PCV. Respiratory parameters were measured by pulmonary monitor(CP-100 pulmonary monitor, Bicore, Irvine, CA, USA). RESULTS: 1) Mean tidal volumes(VT) in each mode were not different(VCV, 431+/-102ml ; PCV, 417+/-99ml; PRVC, 414+/-97ml) 2) The coefficient of variation(CV) of VT were 5.2+/-3.9% in VCV, 15.2+/-7.5% in PCV and 19.3+/-10.0% in PRVC. The CV of VT in PCV and PRVC were significantly greater than that in VCV(p<0.01). 3) Mean peak inspiratory pressure(PIP) in VCV(31.0+/-6.9cm HD) was higher than PIP in PCV(26.0+/-6.5cm H20) or PRVC(27.0+/-6.4cm HD)(p<0.05). 4) The CV of PIP were 13.9+/-3.7% in VCV, 4.9+/-2.6% in PVC and 12.2+/-7.0% in PRVC. The CV of PIP in VCV and PRVC were greater than that in PCV(p<0.01). CONCLUSIONS: Because of wide fluctuations of VT and PIP, PRVC mode did not seem to have advantages compared to VCV or PCV in the patients with unstable respiratory mechanics.
Acute Lung Injury ; Barotrauma ; Electric Impedance ; Humans ; Respiration, Artificial ; Respiratory Mechanics* ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury

BACKGROUND: Experimentally, maintaining high pressure or high volume ventilation in animal models produces an acute lung injury, however, there was little information on remodeling. We investigated the collagen synthesis in a rat model of ventilator-induced lung injury. METHODS: Rats were ventilated with room air at 85 breaths/minute for 2 hours either tidal volume 7 ml/kg or 20 ml/kg (V(T)7 or V(T)20, respectively). After 2 hours of ventilation, rats were placed in the chamber for 24 hours. Lung collagen was evaluated by immunohistochemistry (n=5) and collagen was quantitated by collagen assay (n=5). Static compliance (Csta) of the whole lung as obtained from the pressure volume curves. RESULTS: Type I collagen was an increase in expression in the interstitium with large V(T) (20 ml/ kg) ventilation after 2 hours of mechanical ventilation (MV), and further increased expression after 24 hours of recovery period. Static lung compliance was significantly (p<0.05) decreased in the V(T)20 compared with V(T)7 (0.221+/-0.05 vs 0.305+/-0.06 ml/cm H2O) after 2 hours of MV. There was a further decrease in lung compliance after 24 hours of recovery period (0.144+/-0.07 vs 0.221+/-0.05, p<0.05) in the V(T)20. CONCLUSIONS: Large tidal volume ventilation causes an increase in type 1 collagen expression with reduction of lung compliance.
Acute Lung Injury ; Animals ; Collagen Type I ; Collagen* ; Compliance ; Immunohistochemistry ; Lung ; Lung Compliance ; Models, Animal* ; Rats* ; Respiration, Artificial ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury*

BACKGROUND: Adaptive support ventilation (ASV), an automated closed-loop ventilation mode, adapts to the mechanical characteristics of the respiratory system by continuous measurement and adjustment of the respiratory parameters. The adequacy of ASV was evaluated in the patients with acute lung injury (ALI). METHODS: A total of 36 patients (19 normal lungs and 17 ALIs) were enrolled. The patients' breathing patterns and respiratory mechanics parameters were recorded under the passive ventilation using the ASV mode. RESULTS: The ALI patients showed lower tidal volumes and higher respiratory rates (RR) compared to patients with normal lungs (7.1+/-0.9 mL/kg vs. 8.6+/-1.3 mL/kg IBW; 19.7+/-4.8 b/min vs. 14.6+/-4.6 b/min; p<0.05, respectively). The expiratory time constant (RCe) was lower in ALI patients than in those with normal lungs, and the expiratory time/RCe was maintained above 3 in both groups. In all patients, RR was correlated with RCe and peak inspiratory flow (rs=-0.40; rs=0.43; p<0.05, respectively). In ALI patients, significant correlations were found between RR and RCe (rs=-0.76, p<0.01), peak inspiratory flow and RR (rs=-0.53, p<0.05), and RCe and peak inspiratory flow (rs=-0.53, p<0.05). CONCLUSION: ASV was found to operate adequately according to the respiratory mechanical characteristics in the ALI patients. Discrepancies with the ARDS Network recommendations, such as a somewhat higher tidal volume, have yet to be addressed in further studies.
Acute Lung Injury ; Automation ; Humans ; Lung ; Respiration ; Respiratory Mechanics ; Respiratory Rate ; Respiratory System ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury ; Ventilators, Mechanical

BACKGROUND: Adaptive support ventilation (ASV), an automated closed-loop ventilation mode, adapts to the mechanical characteristics of the respiratory system by continuous measurement and adjustment of the respiratory parameters. The adequacy of ASV was evaluated in the patients with acute lung injury (ALI). METHODS: A total of 36 patients (19 normal lungs and 17 ALIs) were enrolled. The patients' breathing patterns and respiratory mechanics parameters were recorded under the passive ventilation using the ASV mode. RESULTS: The ALI patients showed lower tidal volumes and higher respiratory rates (RR) compared to patients with normal lungs (7.1+/-0.9 mL/kg vs. 8.6+/-1.3 mL/kg IBW; 19.7+/-4.8 b/min vs. 14.6+/-4.6 b/min; p<0.05, respectively). The expiratory time constant (RCe) was lower in ALI patients than in those with normal lungs, and the expiratory time/RCe was maintained above 3 in both groups. In all patients, RR was correlated with RCe and peak inspiratory flow (rs=-0.40; rs=0.43; p<0.05, respectively). In ALI patients, significant correlations were found between RR and RCe (rs=-0.76, p<0.01), peak inspiratory flow and RR (rs=-0.53, p<0.05), and RCe and peak inspiratory flow (rs=-0.53, p<0.05). CONCLUSION: ASV was found to operate adequately according to the respiratory mechanical characteristics in the ALI patients. Discrepancies with the ARDS Network recommendations, such as a somewhat higher tidal volume, have yet to be addressed in further studies.
Acute Lung Injury ; Automation ; Humans ; Lung ; Respiration ; Respiratory Mechanics ; Respiratory Rate ; Respiratory System ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury ; Ventilators, Mechanical