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High-frequency ventilation has been an unconventional option for more than three decades and during that period several varieties of high-frequency ventilators have come and gone. Currently, interest in high-frequency ventilation in adult critical care is part of a larger search for ventilator strategies that can support gas exchange in the severely hypoxemic patient without contributing additional ventilator-induced lung injury. Over the past 30 years, high-frequency ventilators provided an experimental tool that identified many of the mechanisms that contribute to ventilator-induced lung injury. It became clear that ventilator-induced lung injury is minimized by ventilator patterns that achieve homogeneous aeration of as much of the lung as possible, avoiding both injury from overdistension (volutrauma) and that arising from the repetitive opening and closing of lung units in regions of atelectasis (atelectrauma) (Fig. 19-1).1 Failure to operate in the “safe zone” initiates biotrauma.2,3

Figure 19-1

Pressure-volume curve of a moderately diseased lung, as in a patient with acute lung injury. Ventilator-induced lung injury occurs at both extremes of lung volume. In the zone of overdistension, damage arises from edema fluid accumulation, surfactant degradation, and mechanical disruption. In the zone of derecruitment and atelectasis, lung injury arises from the direct trauma of repeated closure and reexpansion of small airways and alveoli, through accumulation and activation of inflammatory cells with release of cytokines (biotrauma), through interactions with local hypoxemia, by inhibition of surfactant, and through compensatory overexpansion of the rest of the lung as the lung “shrinks.” High end-expiratory pressures plus small tidal volume cycles are needed to stay in the safe window. (Reproduced, with permission, from Lippincott Williams & Wilkins, Froese AB, High-frequency oscillatory ventilation for adult respiratory distress syndrome: let’s get it right this time. Crit Care Med. 1997;25:906–908.)

The concept of a “safe zone” within which to ventilate the atelectasis-prone lung has been reflected in numerous clinical trials of lung-protective ventilation over the last 15 years. Conventional ventilator protocols have found survival benefit from shrinking the tidal volume and minimizing peak or plateau distending pressures.4 Studies such as that of Roupie et al5 and Terragni et al6 suggest that very small tidal volumes—even lower than 6 mL/kg predicted body weight—may be needed in some patients (those with the worst lung injury) to avoid overdistension. Very high levels of positive end-expiratory pressure (PEEP) would be needed in some patients to avoid derecruitment.7 Concurrently, high-frequency ventilation—both in oscillatory and jet forms—has become an established lung-protective modality in neonatal and pediatric intensive care (see Chapter 23).814 The question, however, persists: in severe acute respiratory distress syndrome in adult patients, will use of a high-frequency device result in clinically important outcome differences compared with lung-protective conventional ventilation, or are newer conventional ventilator protocols now equally able to protect the lung?1517

Several existing reviews detail the history of ...

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