Did studies on HFOV fail to improve ARDS survival because they did not decrease VILI? On the potential validity of a physiological concept enounced several decades ago

Abstract

High frequency oscillatory ventilation (HFOV) has been the subject of extensive physiological research for 30 years and even more so of an intense debate on its potential usefulness in the treatment of acute respiratory distress syndrome (ARDS). This technique has been enthusiastically promoted by some teams until two high-quality randomized clinical trials in adults with ARDS showed that HFOV did not decrease and might have even increased mortality. As a consequence of these results, physiological concepts such as atelectrauma and biotrauma on which ARDS management with HFOV were based should be reexamined. In contrast, the concept of volutrauma, i.e., end-inspiratory overdistension, as the cause for ventilator-induced lung injury might help explain excess mortality during mechanical ventilation of ARDS when inspiratory volumes are too high. This is what might have happened during one of the recent studies on HFOV. Failure of this complex technique must be put in perspective with the dramatic improvement of ARDS prognosis with very simple interventions such as tidal volume reduction, early pharmacological paralysis, and prone positioning which all limited end-inspiratory volume.

High frequency oscillatory ventilation for adult ARDS: Is this the end of the road?

“…These results are disappointing for clinicians who have HFOV in their armamentarium for the management of moderate to severe acute respiratory distress syndrome (ARDS) in adults. However, as both trials possess the strength of being well-conducted prospective, randomized, controlled, multicenter, multinational studies, their results could be translated to general application in similar populations.Despite the theoretical advantage of less volutrauma and atelectrauma by the use of HFOV, there is growing evidence that ventilator-induced lung injury (VILI) still occurs due to continuous overdistension with high pressure, as well as oscillation amplitude and frequency related biotrauma [3]. Is the VILI the only responsible factor for the failure of HFOV?…”

“…Despite the theoretical advantage of less volutrauma and atelectrauma by the use of HFOV, there is growing evidence that ventilator-induced lung injury (VILI) still occurs due to continuous overdistension with high pressure, as well as oscillation amplitude and frequency related biotrauma [3]. Is the VILI the only responsible factor for the failure of HFOV?…”

Does high-pressure, high-frequency oscillation shake the foundations of lung protection?

“…But with such critical elements respected and most unstable units held open, it seems reasonable that high-frequency oscillation (HFO), a strategy that targets reduced tidal volume and open lung, should be nearly ideal as a lungprotective methodology. It was therefore upsetting that a rigorously designed and executed clinical trial demonstrated that HFO could increase mortality risk [5].In this issue of Intensive Care Medicine, pioneering contributors to VILI research (Didier Dreyfuss and colleagues) present a cogent, detailed, and deliberately provocative argument that the cause of this unexpected result might be violation of the basic directive to avoid high airway pressures, with the likely mechanism being sustained and excessive tissue stretch [6]. The implication is that opening/closure and stress focusing, though acknowledged contributors to VILI at conventional ventilation frequencies, have received disproportionate attention.…”

“…In this issue of Intensive Care Medicine, pioneering contributors to VILI research (Didier Dreyfuss and colleagues) present a cogent, detailed, and deliberately provocative argument that the cause of this unexpected result might be violation of the basic directive to avoid high airway pressures, with the likely mechanism being sustained and excessive tissue stretch [6]. The implication is that opening/closure and stress focusing, though acknowledged contributors to VILI at conventional ventilation frequencies, have received disproportionate attention.…”

“…We also know that minimizing contributors to stress amplification-mechanical heterogeneity (e.g., with adequate PEEP and prone positioning) is likely to pay dividends, especially when transpulmonary forces are high and background conditions are conducive to VILI expression. Dreyfuss and colleagues [6] are quite correct in asserting that one of the key principles of lung protection-avoidance of high transalveolar pressure-was compromised by OSCIL-LATE's focus on open lungs and small tidal volumes. But whether tissue tensions, DPs, and delivered power were lung damaging has not been settled.…”