Indian Journal of Anaesthesia

EDITORIAL
Year
: 2008  |  Volume : 52  |  Issue : 4  |  Page : 363-

Ventilator-Induced Lung Injury


Pramila Bajaj 
 Editor, IJA, India

Correspondence Address:
Pramila Bajaj
Editor, IJA
India




How to cite this article:
Bajaj P. Ventilator-Induced Lung Injury.Indian J Anaesth 2008;52:363-363


How to cite this URL:
Bajaj P. Ventilator-Induced Lung Injury. Indian J Anaesth [serial online] 2008 [cited 2020 Sep 22 ];52:363-363
Available from: http://www.ijaweb.org/text.asp?2008/52/4/363/60649


Full Text

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 [1] . 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 [2],[3] . 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 [4] .

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 [5],[6],[7] is not specific. It closely resembles that observed during human ARDS [8] . 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 [9],[10],[11] .

In light microscopy studies, interstitial and alveolar oedemas have been reported after mechanical ventilation with high peak airway pressure [5],[9]. 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 [12],[13] .

Clinicians quickly recognised that mechanical ventilation could cause disruption of the air space wall and leakage of air, the so-called barotrauma [14] . 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 [15],[16] , 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) [9],[17] . 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[9] . 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[21] . 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[21],[22] . 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[23],[24] . 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[25],[26] as a result of alveolar-capillary barrier damage. The administration of PEEP diminishes this effect[26] . Adverse ventilatory strategies may also affect the pulmonary-to-systemic translocation of endotoxin[27] . Ventilator-induced high plasma levels of endotoxin and bacteria are associated with an increased mortality rate[27],[28] .

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[29] . 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[29] . Finally, it is well known that the dysregulation of apoptotic pathways can contribute to the epithelial injury observed in patients with ARDS[30] .

References

1Ashbaugh DG, Bigelow DB, Petty TL, et al. Acute respiratory distress in adults. Lancet 1967;2:319-323.
2Parker JC, Hernandez LA, Peevy KJ. Mechanisms of ventilator-induced lung injury. Crit Care Med 1993;21:131-143.
3Tsuno K, Miura K, Takey M, et al. Histopathologic pulmonary changes from mechanical ventilation at high peak airway pressures. Am Rev Respir Dis 1991; 143:1115-1120.
4Gammon RB, Shin MS, Groves RH Jr, et al. Clinical risk factors for pulmonary barotrauma: a multivariate analysis. Am J Respir Crit Care Med 1995;152:1235-1240.
5Dreyfuss D, Basset G, Soler P, et al. Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in, rats. Am Rev Respir Dis 1985;132:880-884.
6Dreyfuss D, Soler P, Basset G, et al. High inflation pressure pulmonary edema: respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis 1988;137:1159-1164.
7Dreyfuss D, Soler P, Saumon G. Spontaneous resolution of pulmonary edema caused by short periods of cyclic overinflation. J Appl Physio 1992;l72:2081-2089.
8Bachofen M, Weibel ER. Structural alterations of lung parenchyma in the adult respiratory distress syndrome. In: Bone RC (ed) Clinics in Chest Medicine. W. B. Saunders, Philadelphia 1982;pp 35-56.
9Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures. Protection by positive end-expiratory pressure. Am Rev Respir Dis 1974; 110:556-565.
10Kolobow T, Moretti MP, Fumagalli R, et al. Severe impairment in lung function induced by high peak airway pressure during mechanical ventilation. Am Rev Respir Dis 1987;135:312-315.
11Tsuno K, Prato P, Kolobow T. Acute lung injury from mechanical ventilation at moderately high airway pressures. J Appl Physiol 1990;69:956-961.
12Staub NC, Nagano H, Pearce ML. Pulmonary edema in dogs, especially the sequence of fluid accumulation in lungs. J Appl Physiol 1967;22:227-240.
13Staub NC. Pulmonary edema. Physiol Rev 1974;54:678-811.
14Macklin MT, Macklin CC. Malignant interstitial emphysema of the lungs and mediastinum as an important occult complica­tion in many respiratory disease and other conditions: an interpretation of clinical literature in the light of laboratory experiment. Medicine 1944; 23:281-352.
15Greenfield LJ, Ebert PA, Benson DW. Effect of positive pressure ventilation on surface tension properties of lung extracts. Anesthesiology 1964; 25:312-316.
16Sladen A, Laver MB, Pontoppidan H. Pulmonary complications and water retention in prolonged mechanical ventilation. N Engl J Med 1968; 279:448-453.
17Dreyfuss D, Saumon G. Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation. Am Rev Respir Dis 1993; 148:1194-1203.
18Sandhar BK, Niblett DJ, Argiras EP, et al. Effects of positive end-expiratory pressure on hyaline membrane formation in rabbit model of the neonatal respiratory distress syndrome. Intensive Care Med 1988;14:538-546.
19Colmenero Ruiz M, Fernandez Mondejar EM, Fernandez Sacristan MA et al. PEEP at low tidal volume ventilation reduce lung water in porcine pulmonary edema. Am J Respir Crit Care Med 1997;155:964-970.
20Bshouty Z, Ali J, Younes M. Effect of tidal volume and PEEP on rate of edema formation in in situ perfused canine lobes. J Appl Physiol 1988; 64:1900-1907.
21Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from barotraumas to biotrauma. Proc Assoc Am Physicians 1998; 110:482-488.
22Uhlig S. Ventilation-induced lung injury and mechanotransduction: stretching it too far? Am J Physiol Lung Cell Mol Physiol 2002;282:L892-L896.
23Slutsky AS, Tremblay LN. Multiple system organ failure. Is mechanical ventilation a contributing factor? Am J Respir Crit Care Med 1998;157:1721-1725.
24Dreyfuss D, Saumon G. From ventilator-induced lung injury to multiple organ dysfunction. Intensive Care Med 1998;24:102-104.
25Nahum A, Hoyt J, Schmitz L, et al. Effect of mechanical ventilation strategy on dissemination of intratracheally instilled Excherichia coli in dogs. Crit Care Med 1997;25:1733-1743.
26Verbrugge SJ, Sorm V, van't VeenA, et al. Lung overinflation without positive end-expiratory pressure promotes bacteremia after experimental Klebsiellapneumoniae inoculation. Intensive Care Med 1998;24: 172-177.
27Murphy DB, Cregg N, Tremblay L, et al. Adverse ventilatory strategy causes pulmonary-to-systemic translocation of endotoxin. Am J Respir Crit Care Med 2000;162:27-33.
28Lin CY, Zhang H, Cheng KC, et al. Mechanical ventilation may increase susceptibility to the development of bacteremia. Crit Care Med 2003;31:1429-1434.
29Imai Y, Parodo J, Kajikawa 0, et al. Injurious mechanical ventilation and end organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA 2003;289:2104-2112.
30Martin TR, Nakamura M, Matute-Bello G The role of apoptosis in acute lung injury. Crit Care Med 2003;31: S 184-S 188.