|Year : 2008 | Volume
| Issue : 4 | Page : 363
Ventilator-Induced Lung Injury
Editor, IJA, India
|Date of Web Publication||19-Mar-2010|
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Bajaj P. Ventilator-Induced Lung Injury. Indian J Anaesth 2008;52:363
Mechanical ventilation is the fundamental technique for life support in the intensive care setting. It is an indispensable tool for providing adequate gas exchange, re-establishing sufficient oxygen supply to peripheral organs, and for resting respiratory muscle in many disease states. The major progress in mechanical ventilation occurred during the poliomyelitis epidemic. However, the greatest impetus for technological advancement followed the description of acute respiratory distress syndrome (ARDS) by Ashbaugh et al in 1967  . ARDS, the most severe form of acute lung injury (All), is a common disease with devastating clinical effects.
Actually, one of the most important concepts in the care of critically ill patients is the recognition that mechanical ventilation can worsen, or even cause, lung injury, a condition referred to as ventilator-induced lung injury (VILI). Research in a number of species has shown that mechanical ventilation itself can lead to lung injury that is functionally and histologically indistinguishable from that seen in ARDS , . The recognition of this similarity between VILI and ARDS has prompted a number of investigators to suggest that ARDS may in part be a product of the ventilatory management in addition to the progression of the underlying disease. VILI is determined by the dynamic and continuous interaction between the mechanical characteristics of the lung and the ventilator settings. Patients with ARDS often have a number of morphological and functional changes (e.g. surfactant dysfunction, underlying lung disease, malnutrition, oxygen toxicity, infection, atelectasis, alveolar oedema) that not only increase the lungs' susceptibility to injury by mechanical ventilation, but also impair the lungs' ability to repair the damage incurred  .
Many studies have sought to identify the risk factors, or the potential adverse effects of various forms of mechanical ventilation, and to develop strategies for preventing VILI. The deleterious effects of mechanical ventilation depend on numerous factors, among which, the level of airway pressure applied and resulting volume changes, the end-expiratory lung volume, the overall lung inflation and the extent of the inflammatory process are the most significant.
The macroscopic and microscopic damage observed in VILI ,, is not specific. It closely resembles that observed during human ARDS  . However, there is a clear relationship between the duration of mechanical ventilation, the level of harmful stimulus, the extent of the injury, and the overall appearance of the lung.
Macroscopically, the lungs of animals injured by adverse ventilatory strategy display focal zones of atelectasis, severe congestion and enlargement because of oedema ,, .
In light microscopy studies, interstitial and alveolar oedemas have been reported after mechanical ventilation with high peak airway pressure ,. The degree of oedema varies with the magnitude of the peak airway pressure and the duration of mechanical ventilation. Oedema is initially confined to the interstitial spaces and is visualised as peribronchovascular cuffs , .
Clinicians quickly recognised that mechanical ventilation could cause disruption of the air space wall and leakage of air, the so-called barotrauma  . VILI was, for years, synonymous with barotrauma. The adverse consequences of these macroscopic events, tension pneumothorax usually obvious, being the most threatening extraalveolar accumulation of air. More subtle physiological and morphological alterations require more time to be recognised. Several early experimental and clinical studies suggested that mechanical ventilation might adversely affect lung function and structure , , but the potential harmful effects remained controversial.
There is a large body of evidence indicating that lung damage may also be caused by ventilation at low lung volume (meaning end-expiratory lung volume). This injury is thought to be related to the cyclic opening and closing of distal airways, ducts and/or alveolar units (hence, the term atelectrauma).
Repeated recruitment-derecruitment of terminal units may lead to potential increased local shear stress, particularly if the event is repeated with each breath. Many authors (using various species, diverse lung injury models and different ventilatory strategies) have demonstrated this kind of injury and/or the potential protective effect of positive end-expiratory pressure (PEEP) , . PEEP application may prevent diffuse alveolar damage by stabilising distal units and maintaining recruitment throughout the ventilatory cycle.
The protective effect of PEEP was first addressed in 1974, in a comprehensive study of intact animals, demonstrating that high inflation-induced lung oedema (45 cmH 2 O) was less severe when PEEP (10 cmH 2 O) was applied . The beneficial effect of PEEP was attributed to reduced lung tissue stress (by decreasing tidal volume) and capillary filtration (at least in part because of haemodynamic depression), as well as to the preservation of surfactant activity. PEEP is also believed to preserve the integrity of the epithelial layer18-20.Lung volume at the end of inspiration (i.e. the overall degree of lung distension) seems to be the main determinant of VILI severity. Application of PEEP may result in lung overinflation if it is followed by a significant change in functional residual capacity owing to the increase in end-inspiratory volume, Additionally, depending on the homogeneity of ventilation distribution, this over-inflation will preferentially affect the more distensible areas.
Mechanical ventilation has also been shown to have significant effects on the amount of inflammatory cells in the lungs and soluble mediators (e.g. cytokines) in lung and systemic circulation, a process that has been termed biotrauma . Both clinical and basic studies have demonstrated that injurious ventilation strategies can initiate or perpetuate local and systemic inflammatory response, which, in turn, can potentially contribute to MSOF, . The main concept is that inflammatory mediators originating in the lung cross an impaired alveolar-capillary barrier and access the circulation, where they potentially exert detrimental effect.
Injurious mechanical ventilation may also promote the translocation of bacteria and/or their products from the lung into the bloodstream, thereby contributing to the development of MSOF, . Overall lung distension associated with the repetitive opening and closing of distal units has been proven to facilitate translocation to the bloodstream of bacteria that had previously been instilled intratracheally, as a result of alveolar-capillary barrier damage. The administration of PEEP diminishes this effect . Adverse ventilatory strategies may also affect the pulmonary-to-systemic translocation of endotoxin . Ventilator-induced high plasma levels of endotoxin and bacteria are associated with an increased mortality rate, .
It has been recently demonstrated that an adverse mechanical strategy can lead to distal organ epithelial cell apoptosis. Circulating proapoptotic soluble 'factors (soluble Fas ligand) produced by injurious ventilatory strategies may be involved in this mechanism. Epithelial cell apoptosis in the kidney and small intestine is increased by injurious ventilatory strategies . Plasma from adversely ventilated animals induced in vitro apoptosis in renal tubular cells, which was reduced by a fusion protein that blocks soluble Fas ligand . Finally, it is well known that the dysregulation of apoptotic pathways can contribute to the epithelial injury observed in patients with ARDS .
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