Ventilator-induced Lung Injury

Abstract

During mechanical ventilation, high end-inspiratory lung volume (whether it be because of large tidal volume (VT) and/or high levels of positive end-expiratory pressure) results in a permeability type pulmonary oedema, called ventilator-induced lung injury (VILI). Previous injury sensitises lung to mechanical ventilation.This experimental concept has recently received a resounding clinical illustration after a 22% reduction of mortality was observed in acute respiratory distress syndrome patients whose VT had been reduced. In addition, it has been suggested that repetitive opening and closing of distal units at low lung volume could induce lung injury but this notion has been challenged both conceptually and clinically after the negative results of the Acute Respiratory Distress Syndrome clinical Network Assessment of Low tidal Volume and Elevated end-expiratory volume to Obviate Lung Injury (ARDSNet ALVEOLI) study.Experimentally and clinically, involvement of inflammatory cytokines in VILI has not been unequivocally demonstrated. Cellular response to mechanical stretch has been increasingly investigated, both on the epithelial and the endothelial side. Lipid membrane trafficking has been thought to be a means by which cells respond to stress failure.Alterations in the respiratory system pressure/volume curve during ventilator-induced lung injury that include decrease in compliance and position of the upper inflection point are due to distal obstruction of airways that reduce aerated lung volume. Information from this curve could help avoid potentially harmful excessive tidal volume reduction. [3][4][5][6][7]. The purpose of this paper is to review the different situations in which VILI can occur based on animal studies and to place these results into a clinical perspective of ventilatory management of acute respiratory distress syndrome (ARDS). Evidence for ventilator-induced lung injury Ventilation of intact lungsHigh lung volume ventilator-induced lung injury. WEBB and TIERNEY [8] were the first to demonstrate that mechanical ventilation could cause pulmonary oedema in intact animals. They were able to show in rats subjected to positive airway pressure ventilation that pulmonary oedema was more severe and occurred more rapidly when the animals were ventilated with 45 cmH 2 O than with 30 cmH 2 O peak airway pressure. Animals ventilated for 1 h with 14 cmH 2 O peak airway pressure did not develop oedema. It was later confirmed that ventilation with high airway pressure produces capillary permeability alterations, nonhydrostatic pulmonary oedema and tissue damage resembling that observed during ARDS [9]. Further studies demonstrated that VILI depended mainly on lung volume and especially on the end-inspiratory volume [10]. The corresponding pressure is termed "plateau" pressure and its clinical importance has been emphasised in a Consensus Conference on mechanical ventilation [11]. The respective roles of increased airway pressure and increased lung volume on the development of VILI were clarified by...

Ventilation-induced lung injury exists in spontaneously breathing patients with acute respiratory failure: No

“…However, there is experimental evidence that SB can also cause or worsen lung injury during mechanical ventilation [6,7] through mechanisms that include negative intrathoracic and increased transalveolar pressure with lack of control of tidal volume (VT), ventilation inhomogeneity and cyclic and static overinflation [8].…”

High frequency oscillation ventilation compared to conventional mechanical ventilation plus exogenous surfactant replacement in rabbits

“…Dependendo do padrão ventilatório adotado, pode-se induzir a lesões pulmonares progressivas. A técnica usada para ventilar áreas de "baixa complacência" pode não ser apropriada para ventilar áreas com "complacência normal", podendo, nestas regiões, induzir a dano pulmonar (VILI -Ventilator Induced Lung Injury) [2][3][4][5][6] .…”

“…Neste caso, os pulmões são ventilados usando baixos volumes correntes, inferiores ao ponto de inflexão da curva pressão volume, e/ou a pressão no final da expiração não é capaz de manter as vias aéreas terminais e alvéolos abertos, levando a progressivo colapso pulmonar, sendo que, para reabrir estas unidades, uma pressão maior será necessária; d) biotrauma, quando a ventilação mecâni-ca causa colapso, estiramento ou ruptura tecidual pulmonar levando a dano celular com aumento dos mediadores inflamatórios locais (citoquinas, radicais livres de oxigê-nio,...) 2,[4][5][6][7] .…”

“…Nos pacientes com SARA, ocorre também disfunção do surfactante, promovendo instabilidade das unidades, alveolares favorecendo ao seu colabamento 3,5,6,10 . A ventilação protetora nesta situação baseia-se em aumentar o volume expiratório pulmonar (por exemplo, aumentando a pressão expiratória positiva final -PEEP) para evitar o colapso alveolar, assim como usar baixos volumes correntes prevenindo a hiperinsuflação (distensão) alveolar.…”

Protektive Beatmung im Operationssaal

“…In kleinen Tieren kann die Beatmung mit exzessiv hohen Tidalvolumina von 30-40 ml/kg-KG sogar das ARDS hervorrufen [6], dies ist der sog. beatmungsinduzierte Lungenschaden ("ventilator induced lung injury", VILI).…”