Many premature infants require mechanical ventilatory support and oxygen supply. Because they have immature lungs, these ventilator supports contribute to the development of ventilator induced lung injury, which causes the development of bronchopulmonary dysplasia (BPD) in large portion. Recent meta-analysis reported that the volume-targeted ventilation reduced the development of BPD and death. Non-invasive ventilator support also can reduce the adverse effects associated with intubation and mechanical ventilatory support. The technological advancements, including microprocessors, enhance the development of new devices with new modes of ventilatory support. A lot of limits and demerits of conventional ventilatory support obviously inspired the thoughts of new modes of ventilatory support. In this article, new modes of ventilatory support for neonates, as well as conventional modes, are introduced in the hope of adopting strategies with evidences efficiently.
Bronchopulmonary Dysplasia ; Humans ; Infant, Newborn ; Infant, Premature ; Intensive Care Units, Neonatal ; Intubation ; Lung ; Microcomputers ; Oxygen ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury ; Ventilators, Mechanical

Positive pressure ventilation (PPV) is one of the most commonly used treatment modalities in the field of neonatology to achieve adequate gas exchange for infants with respiratory difficulties. However, mechanical ventilation may cause lung injury through various mechanisms, including high airway pressure and high tidal volume, leading to acute respiratory distress syndrome, bronchopulmonary dysplasia or multiple organ failure. To prevent these injuries, clinicians, especially neonatologists, treating premature infants with respiratory distress syndrome, should be familiar with ventilator-induced lung injury and its preventive strategies. In this review, the mechanisms of lung injury, the effects of mechanical ventilation on pulmonary microvascular endothelium, extracelluar matrix and alveolar epithelium, and lung protective strategies of conventional ventilation are introduced. Several forms of conventional ventilation for preterm infants are also described.
Acute Lung Injury ; Bronchopulmonary Dysplasia ; Endothelium ; Epithelium ; Humans ; Infant ; Infant, Newborn ; Infant, Premature ; Lung ; Lung Injury ; Multiple Organ Failure ; Neonatology ; Positive-Pressure Respiration ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury

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

The incidence of bronchopulmonary dysplasia (BPD) has not decreased over the last decade. The most important way to decrease BPD is by weaning the patient from the ventilator as soon as possible in order to reduce ventilator-induced lung injury that underlies BPD, and by using a noninvasive ventilator (NIV). Use of a heated, humidified, high flow nasal cannula (HHHFNC), which is the most recently introduced NIV mode for respiratory support in preterm infants, is rapidly increasing in many neonatal intensive care units due to the technical ease of use without sealing, and the attending physician's preference compared to other NIV modes. A number of studies have shown that nasal breakdown and neonatal complications were lower when using a HHHFNC than when using nasal continuous positive airway pressure (nCPAP), or nasal intermittent positive pressure ventilation. The rates of extubation failure during respiratory support were not different between patients who used HHHFNC and nCPAP. However, data from the use of HHHFNC as the initial respiratory support "after birth", particularly in extremely preterm infants, are lacking. Although the HHHFNC is efficacious and safe, large randomized controlled trials are needed before the HHHFNC can be considered an NIV standard, particularly for extremely preterm infants.
Bronchopulmonary Dysplasia ; Catheters* ; Continuous Positive Airway Pressure ; Hot Temperature* ; Humans ; Incidence ; Infant, Extremely Premature ; Infant, Newborn ; Infant, Premature* ; Intensive Care Units, Neonatal ; Intermittent Positive-Pressure Ventilation ; Noninvasive Ventilation ; Ventilator-Induced Lung Injury ; Ventilators, Mechanical ; Weaning

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

The ventilator-induced lung injury (VILI) was centered on the "static" characteristics of the mechanical ventilation in early phases (tidal volume, plateau pressure, positive end-expiratory pressure and driving pressure). But the "dynamic" characteristics of ventilation must not be ignored (respiratory rate and flow). Mechanical energy and mechanical power (the pace of performing energy load) regarding all factor have won wide spread attention. The energy generated by mechanical ventilation is mainly used to expand respiratory system and overcome resistance, a fraction of energy acts on lung tissues probably inducing "heat" and inflammation that is related to lung injury. The review described recent conceptual advances regarding the mechanical energy and power, and the relationship with VILI, hoping to help further understanding the risk factors for VILI.
Humans ; Lung ; Positive-Pressure Respiration ; Respiration, Artificial ; Respiratory Distress Syndrome ; Tidal Volume ; Ventilator-Induced Lung Injury

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

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

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

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