The basic principles of managing acute lung injury (ALI) are well known.

The basic principles of managing acute lung injury (ALI) are well known. However, improved understanding of the potential for ventilator-induced lung damage has inspired a number of well-reasoned therapeutic innovations whose value publicly remains unproven. The purpose of this discussion is to briefly review the basis for make anxious regarding the traditional approach to mechanical ventilation and drawing from this evidence to propose a ventilatory strategy consistent with elucidation principles emerging from the incomplete data base at hand. From the entrance it should be understood that however rational newer approaches might appear, and however consistent the experimental evidence may be, the benefit of altering traditional strategy has not now been rigorously demonstrated in the clinical setting.

TRADITIONAL APPROACH TO MECHANICAL VENTILATION

in the greatest degree traditional ventilatory strategies used in acute intensive care evolv from anesthetic practice. When the lung are uninjured and their capacity to expand is relatively normal, as they commonly are in the perioperative period, tidal turns (VT) of 10 to 15 ml/kg are appropriate to debar the microatelectasis that accompanies monotonous shallow breathing. Respiratory rate is adjusted to "normalize" pH and/or [PaCO.sub.2],[1] and sufficient positive end-expiratory crushing (PEEP) is used to achieve acceptable [Osub2] delivery at nontoxic concentrations of inspired [Osub2] ([FIO.sub.2]). As a mastery airway pressures are monitored yet not rigidly constrained. With not many modifications, this high tidal contortion normoxic, normocapnic ventilation paradigm has become the standard approach to supporting greatest in quantity critically ill patients, including those with ALI. Consequently VT exceeding 800 ml and peak tidal alveolar influences exceeding 50 cm [H.sub.2]O are commonplace in many intensive care environments. Many practitioners advocate using the least chirp consistent with acceptable arterial oxygenation.[2] Clinical observations, as well as disturbing experimental data, strenuously suggest that such an approach may bring the injured lung at risk for further damage.

VENTILATOR-INDUCED LUNG DAMAGE

Several previously unreported forms of ventilator-induced lung damage are now known to appear commonly during the management of ALI. These include interstitial emphysema, tension gas pouch injury to small and terminal bronchi, and lung edema. It is evident that the pathologic findings of ALI are not homogeneously distributed. Although injury may be widespread, gravitationally pendent areas appear edematous and atelectatic, whereas nondependent regions protect to aerate better, at least early in the course.[3] Initially, an of these radiographic changes can be altered on changes of position.[4]

merely a fraction of the injured lung is accessible to gas; in austere cases, no more than common third of all alveoli remain patent. Given that ventilated lung units may retain nearly normal elastance and fragility, the apparent "stiffness" of the lung in ALI is better explained by dint of the presence of fewer functioning alveoli than by dint of a generalized increase in recoil tension.[5] Because the functional compartment has reduc capacity to expand if it were not that must receive the entire tidal dimensions normal tidal volumes may expose it to overdistention, local hyperventilation, and inhibition or depletion of surfactant.[6] Injury may also be the effect from rapid inflation to high transalveolar presss Particularly intense shearing forces may unravel at the junctions of arrangements that are mobile (aerated alveoli) with those that are immobile (collapsed or consolidated alveoli, conducting airways).[7] Any turn for damage is likely to be accentuated from increases in cycling frequency.

Adhesed walls of collapsed bronchi repeatedly require extraordinary pressures to separate; formerly opened, however, much lower squeezings retain patency. If the terminal airways remain clos their unsupported walls may be enslaveed to forces that approach the dynamic presss applied to more central cartilaginous airways. Bronchial damage may come much more frequently than generally appreciated (Fig 1) A modern autopsy study, for example, discovered bronchiolar dilatation, lung cyst formation, and/or microabscesses in 19 of 23 patients with ALI ventilated for prolix periods with peak airway hurrys considered modest ([unkeyable] 38 cm [Hsub2]O) from traditional clinical standards.[8]

Evidence for pressure-induced damage to the alveolar-capillary membrane has been infered by a number of investigators.[9,10] In diverse animal examples transalveolar cycling pressures approximating those corresponding to total lung capacity ([unkeyable] 35 cm [Hsub2]O) can diffusely injure previously normal alveoli above 15- to 60-min periods;[6,11,12] when sustained for several days, on the same level lower peak airway pressures ([les than or equal to] 30 cm [Hsub2]O) can damage normal lung tissues or furnish lung edema.[13] Microscopic injury to the endothelial membrane may be modulated by way of factors that influence transmural capillary pressure[14] Electron-microscopic evidence forcibly suggests that physical breaks in the gas-blood interface appear when transmural capillary pressures are excessive. This line of investigation, which analyzes the enigma of barotrauma in terms of capillary stres failure and transvascular (rather than transalveolar) press is discussed extensively in this issue through Mathieu-Costello and West. Noxious stimuli may be additive; at least single study suggests that two factors acting in combination may bring forth injury that neither alone could inflict.[15]

...