Numerous experimental studies demonstrate the potential for adversepatterns of mechanical ventilation to initiate acute lung injury that characterized by proteinaceous edema. Inflammation and hemorrhage. The great majority of these investigations into ventilator-induced lung injury VILI have focused on the characteristics of the individual cycle tidal volumeinspiratory flow rate and end-expiratory air-way pressure PEEP. Altough these features are of unquestioned importance other characteristics of the clinical environment have been shown to modify the intensity and or nature of the resulting damage.
In the largest and perhaps the most widely cited clinical trial of ventilator strategy in acute lung injury yer undertaken smaller tidal volumes wereassociated whit reduced mortality. This result was attributed to the generally lower peak alveolar pressures and reduced mechanical stresses associated with smaller tidal volumes. Analysis of the date pooled from both trial groups not only demonstrated a positive correlation between plateau pressure and mortality rate but also revealed its monotonic linear nature- without an obvius break pointdown to pressures that are considerably lower than those that are feasible to use feasible to use in the manangement of SDRA. Although such an association does not confirm plateau pressure as the sole causative variable it implies that there may be no safe plateau pressure below which mortality cannot be influenced by further pressure reduction. This observation underscores the need to identifyany cofactors that influence VILI expression.
To this time almost all strategies proposed to limit VILI have altered the ventilator variables associated woht a single tidal cycle. Lower tidal volume lower plateau pressures and higher PEEP settings have ben used to avoid VILI decrease length of ICU stay and curtail the associated mortalty rate. Although less well studie lung injury arising in thecourse of mechanical ventilation may also relate to such non ventilatory factors as body position PaCO2 acid-base state pulmonary vascular pressure changes body temperature concomitant pathologies and pharmacologic agents. In this discussion we review a selected subset of these non ventilatory factors and propose mechanims for their actions. Our objecutive is to focus on those amenable tomodification at the bedside.
PATHOFHYSIOLOGY OF VENTILATION INDUCED LUNG INJURY
Although VILI is a complex process initiated and propagated through several mechanisms generally speaking damage resulting from excessive mechanical stress can be classified into two broad categories structural and inflammatory. The injury process is iniatiaded by mechanical stress and depends on the magnitude frequencyand cumulative effect of this stimulus. Repetitive over stretching and cyclic recruitment-derecritment of collapsed areas that are exposed periodically to high pressure favor injury that disrupts the integrity of the epithelial membrane.
Simultaneously these mechanical forces activate intracellular signaling cascades within ephitelial cells. This activation culminates in recruitment ofpolymorphonuclear leucocytes production of pro-inflamatory cytokines vasodilatation and alveolar edema- collectively a process termed biotrauma once formed alveolar edema has two opposing effects. On one hand completely flooded alveoli are theoretically subject to lower shearing stresses than atelectatic units as the gas-liquid interface is eliminated and alveolar dimensions increase. Furthermoredecreased surface tension in partially flooded units would cause capillaries that are fully embedded in the alveolar walls to bulge into the interior encouraging their rupture. On the other hand the increased weight of the edematous lung may promote small airway compression and accentuate the tendency for tidal opening and closure to occur. If alveolar units do not have enough time to recover...