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[Blue Journal述评]:ARDS的高频振荡通气:演员已经谢幕
2017年10月12日 研究点评, 进展交流 暂无评论

High-Frequency Oscillation in Acute Respiratory Distress Syndrome: The End of the Story?

Vincent JL.

Am J Respir Crit Care Med 2017; 196: 670-671

Acute respiratory distress syndrome (ARDS) is still associated with considerable morbidity and mortality (1). It is characterized by acute onset of diffuse inflammatory lung injury, which causes increased pulmonary vascular permeability, leading to increased lung weight, loss of aerated lung tissue, decreased lung compliance, and increased physiological dead space; the end result is severe hypoxemia. It is well established that mechanical ventilation can aggravate the lesions of ARDS, in a process called ventilator-induced lung injury (VILI). VILI has been attributed primarily to excessive tidal volumes; increased alveolar collapse (atelectrauma) may also contribute. In patients receiving mechanical ventilation, attempts are therefore made to minimize VILI by reducing alveolar overdistension (stress and strain) using application of a sufficient level of positive end-expiratory pressure to prevent atelectrauma.

High-frequency oscillatory ventilation (HFOV) is conceptually an appealing method of mechanical ventilation for patients with ARDS, maintaining gas exchange with a small tidal volume, increased intrathoracic pressure, and reduced alveolar collapse. The adult ventilator is essentially a high-flow continuous positive airway pressure system with the superimposed generation of oscillations through large membrane diaphragms, like a magnet audio loudspeaker cone. The frequency and magnitude of the oscillations can be varied to generate different tidal volume and minute ventilation; frequency is typically set between 5 and 10 oscillations per second. Arterial oxygenation during HFOV can be regulated by adjusting the FIO2 and/or by increasing mean airway pressure.

Two large multicenter randomized controlled trials have been conducted that compared HFOV with conventional lung-protective ventilation: the OSCILLATE (Oscillation for Acute Respiratory Distress Syndrome Treated Early) (2) and OSCAR (Oscillation in ARDS) (3) trials. In the OSCILLATE trial (2), designed to study target lung recruitment with an “open lung approach” and high mean airway pressure, there was higher mortality in the HFOV group than in a group managed with a conventional lungprotective mechanical ventilation strategy (in-hospital mortality, 47 vs. 35%; relative risk of death, 1.33; 95% confidence interval, 1.09–1.64), so that the study, designed to recruit 1,200 patients, was stopped for safety concerns after randomization of 548 patients on the recommendation of the Data and Safety Monitoring Board. In the OSCAR trial (3), designed as a more pragmatic study, there were no differences in mortality rates between the groups. The higher mortality observed in the OSCILLATE trial may have been due to hemodynamic compromise, which can contribute to distant organ failure. Indeed, the mean airway pressure was higher in the OSCILLATE trial than in the OSCAR trial (31+/-2.6 cm H2O vs. 26.9+/-6.2 cm H2O), and the initiation of HFOV in the OSCILLATE trial was associated with increased use of vasoactive support. Another negative effect of HFOV is the increased requirement for sedative agents to improve tolerance to the unusual settings. One cannot argue that OSCILLATE included centers with less experience, because the participating centers had more experience with HFOV than those that participated in the OSCAR trial. Not surprisingly, recent meta-analyses have shown no differences in mortality with HFOV (4, 5).

In this issue of the Journal, Meade and coworkers (pp. 727–733) (6) reviewed the data from 1,552 patients enrolled in four trials, including the large OSCILLATE (548 patients) and OSCAR (795 patients) trials and two smaller trials, the MOAT (Multicenter Oscillatory Ventilation for Acute Respiratory Distress Syndrome Trial; 148 patients) (7) and EMOAT (European Multicenter Oscillator ARDS Trial; 61 patients) studies (8). Again, there were no significant differences in 30-day mortality (40.9% for patients receiving HFOV vs. 37.6% in the control groups; P = 0.16). The interesting sophisticated analysis provided by Meade and colleagues (6) revealed a highly significant interaction between baseline PaO2/FIO2 and the effect of HFOV (P = 0.0003), with increasing harm from HFOV at higher PaO2/FIO2 values. The implications of these findings are that HFOV could potentially still have a place as rescue therapy in severe cases of ARDS (PaO2/FIO2,100 mm Hg), especially when extracorporeal membrane oxygenation (ECMO) is not readily available. The authors’ interpretation of the results is prudent, and I agree with it.

So, is there really a place for HFOV in the management of ARDS? A first question is whether we are ready to perform another clinical trial in these extreme conditions to provide more convincing supportive arguments. The answer is probably no, because patient enrollment in such a trial would be problematic, especially now that ECMO is increasingly available and most such patients could be transferred to ECMO centers when necessary. A second question then is whether HFOV could be used as rescue therapy without performing a further trial. This is also unlikely, because HFOV use would be limited to a small patient population, representing just a few patients a year for most centers and not providing sufficient experience for physicians and nurses to be able to perform HFOV optimally. There are only two ventilators available for HFOV in adults: the Sensormedics 3100B (Yorba Linda, CA), introduced 20 years ago, and the Novalung Vision alpha (Talheim, Germany) or Metran R100 (Kawaguchi, Japan), which has been introduced more recently. It is unlikely that hospitals will be willing to buy these respirators for such limited use. Accordingly, I am afraid this may very well be the end of HFOV in ARDS.

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