It has recently been shown that strategies aimed at preventing ventilator-induced lung injury, such as ventilating with low tidal volumes, can reduce mortality in patients with acute respiratory distress syndrome ARDS.
High-frequency oscillatory ventilation HFOV seems ideally suited as a lung-protective strategy for these patients. HFOV provides both active inspiration and expiration at frequencies generally between 3 and 10 Hz in adults. The amount of gas that enters and exits the lung with each oscillation is frequently below the anatomic dead space. Despite this, gas exchange occurs and potential adverse effects of conventional ventilation, such as overdistension and the repetitive opening and closing of collapsed lung units, are arguably mitigated.
Although many investigators have studied the merits of HFOV in neonates and in pediatric populations, evidence for its use in adults with ARDS is limited.
A recent multicenter, randomized, controlled trial has shown that HFOV, when used early in ARDS, is at least equivalent to conventional ventilation and may have beneficial effects on mortality. The development of the positive pressure mechanical ventilator in the s marked a significant achievement in the care of patients with respiratory failure, and was a cornerstone in the establishment of the discipline of critical care medicine.
Since then, we have learned that although mechanical ventilation is often life saving, it can also be injurious, especially in patients suffering from acute respiratory distress syndrome ARDS [ 1 ].
ARDS can also result in refractory hypoxemia, which can often stimulate attempting nonconventional ventilation strategies such as using nitric oxide, recruitment maneuvers, or prone positioning. Moreover, given that it appears to injure the lung less than conventional modes of ventilation, it may also be ideally suited to use early in ARDS. HFOV fits within the spectrum of the other high-frequency ventilation modes whose common underlying concept is the delivery of breaths at high frequencies and low tidal volumes V t , which are often below the anatomic dead space.
The high-frequency modes are generally divided into those in which the expiratory phase is passive and those in which expiration is active. High-frequency jet ventilation and high-frequency positive pressure ventilation are examples of devices employing passive expiration. Although theoretically attractive, this mode seems to offer little advantage over conventional ventilation in patients with lung injury and, as such, application is limited.
In high-frequency jet ventilation, gas is delivered through a small cannula under high pressures 70— kPa and, combined with entrainment of humidified gas by the Venturi effect, adequate tidal volumes are achieved. Although high-frequency jet ventilation is sometimes used in patients with bronchopleural fistulae, most centers limit their use to rescue situations. For more detailed reviews of these modes of ventilation, the reader is referred to a few of the many reviews on these topics [ 2 , 3 ].
HFOV is similar to other high-frequency modes in that effective oxygenation is achieved by the application of high mean airway pressure P aw. As previously discussed, however, HFOV differs in that expiration is an active process controlled by the ventilator. Theoretically, this results in improved CO 2 elimination and reduced gas trapping.
The present article reviews the rationale for the use of HFOV as a ventilatory strategy in adults, reviews practical issues for intensivists using this modality, and reviews the evidence supporting its use in adult patients with ARDS. Despite the fact that patients with respiratory failure often require positive pressure mechanical ventilation, it has become clear that mechanical ventilation using conventional strategies can be harmful.
Gross barotrauma resulting in extraparenchymal air in the forms of pneumothorax, pneumomediastinum, or subcutaneous emphysema are obvious examples of the detrimental effects of mechanical ventilation [ 4 ]. However, more subtle microscopic damage can also occur in lungs that have been subjected to mechanical ventilation.
This damage has been termed ventilator-induced lung injury, and can mimic the histological, radiographic, and clinical changes that occur in patients with ARDS [ 5 ]. The damage is thought to result from excess airway pressures barotrauma , from high lung volumes volutrauma , or from the repetitive opening and closing of collapsed lung units with successive tidal breaths atelectrauma [ 6 ]. Evidence for this comes from numerous studies in animals, which have shown that the ventilator can induce pathologic changes in normal lungs and have shown that strategies minimizing these effects are beneficial [ 6 - 9 ].
In addition, we now know that lung injury itself ventilator induced or otherwise can propagate the proinflammatory cytokine cascade biotrauma and can contribute to the development of multisystem organ failure in humans with ARDS [ 10 , 11 ].
It is important to note that multisystem organ failure is often the cause of death in those patients that die from ARDS [ 12 - 14 ]. Previous ventilator strategies have focused on normalization of arterial blood gases [ 15 ]. The tidal volumes and subsequent airway pressures needed to achieve these goals are typically safe in normal lungs; however, it is currently felt that these levels are probably injurious in patients with lung injury, where the same volumes are delivered to a much smaller lung volume, resulting in overdistension [ 16 ].
Two large randomized, controlled trials in humans with ARDS have shown that ventilatory strategies limiting overdistension using low tidal volumes can have a mortality benefit [ 17 , 18 ].
One of these studies also included efforts to recruit collapsed lung units and to keep these units open [ 18 ].
The benefit of 'opening' the lung either with recruitment maneuvers, with application of higher levels of positive end-expiratory pressure PEEP , or with high P aw , such as that achieved with HFOV, is more controversial because recruitment with any of these strategies can result in overdistension of more 'normal' lung regions.
Overall, the use of these techniques is supported by a large body of animal literature for the use of PEEP [ 19 - 22 ] and, to a lesser degree, by clinical trials [ 18 , 23 , 24 ]. There is also some suggestion that the benefit of recruitment maneuvers themselves depends on several patient-specific factors [ 25 ]. Lung protective strategies in ARDS are currently aimed at reducing plateau airway pressures and tidal volumes, and at attempting to have an open lung [ 26 ].
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Based on this rationale, the high P aw in conjunction with small V t values appears to make HFOV ideally suited as a lung protective strategy. The potential of high-frequency ventilation in humans has been studied since the observation that adequate gas exchange occurred in panting dogs with tidal volumes lower than the anatomic dead space [ 27 ]. In the s, groups in Germany and Canada found a system that oscillated gas into and out of an animal's lungs was effective at CO 2 elimination [ 28 , 29 ].
Commercial products are now available for children and for adults. These ventilators operate on the following principle Fig. A bias flow of fresh, heated, humidified gas is provided across the proximal endotracheal tube. An oscillating piston pump akin to the woofer of a loudspeaker vibrates this pressurized, flowing gas at a frequency that is generally set between 3 and 10 Hz.
A portion of this flow is thereby pumped into and out of the patient by the oscillating piston. The P aw achieved is sensitive to the rate of bias flow but can be adjusted by varying the back pressure on the mushroom valve through which the bias flow vents into the room.
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The P aw can thus be modified by either adjusting the bias flow rate or the back pressure. Schematic representing the major functioning parts of the high-frequency oscillatory ventilator. See text for a detailed explanation.
The set power on the ventilator controls the distance that the piston pump moves and, hence, controls the tidal volume. The result is a visible wiggle of the patient's body, which is typically titrated to achieve acceptable CO 2 elimination.
These pressures are generally greatly attenuated through the endotracheal tube and larger airways so the press ure swings in the alveoli are much less.
The P aw , on the other hand, is believed to be similar in the ventilator circuit and the alveoli. It seems counterintuitive that reductions in frequency would improve alveolar ventilation; however, HFOV differs from conventional ventilation in that the lung never achieves an equilibrium volume during inspiration and expiration.
Lowering the frequency therefore allows more time for a larger V t to occur.
With HFOV, CO 2 elimination is proportional to the V t and the frequency, but increases in the V t achieved by lowering the frequency are thought to more than compensate for the reduction in frequency. It is also important to note that the actual V t received by the patient depends on a number of factors, including the size of the endotracheal tube, the airway resistance, and the compliance of the total respiratory system.
In addition, the V t can change on a breath-to-breath basis, and therefore ventilator settings are used with clinical factors such as the amount of wiggle in monitoring the patient. As with conventional ventilation, oxygenation is primarily determined by the P aw , by the lung volume, and by the fractional inspired concentration of oxygen FiO 2.
High frequency ventilation (HFV)
The initial settings are typically chosen to achieve a P aw value roughly 5 cmH 2 O greater than that achieved with conventional ventilation. Failure to adequately oxygenate the patient is frequently remedied by increasing the P aw or the FiO 2.
There is no evidence guiding exactly how ventilator adjustments should be made in the hypoxemic patient on HFOV. These increases are made slowly to give time for alveolar recruitment and to assess for cardiovascular impairment.
In addition, these increases are frequently made in conjunction with a recruitment maneuver. P aw values as high as 35—45 cmH 2 O have been used and tolerated [ 30 , 31 ].
In our experience, a higher P aw may result in hemodynamic impairment, especially if the intravascular volume is inadequate.
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Should significant derecruitment from oscillator disconnects or circuit changes occur, our experience suggests that recruitment maneuvers are also helpful in this situation. Many pediatric and adult trials using HFOV discussed later , however, have not utilized such an approach.
Once the patient improves and the FiO 2 can be decreased to below 0. As already described, one of the theoretical advantages of HFOV over other high-frequency modes is the decoupling of oxygenation and CO 2 elimination.
Ventilation is determined by changes in power a surrogate for V t and in frequency. Simply increasing the power will often result in improved ventilation.
Once this is maximized, the frequency can be reduced. One must, however, keep in mind that these steps may lead to larger tidal volumes as already mentioned and to larger pressure swings at the alveoli, and as a result may lead to the potential to negatively impact on lung protection [ 30 - 32 ].
Finally, deflation of the endotracheal tube cuff may help eliminate CO 2 by allowing the front of fresh gas to be advanced to the distal end of the endotracheal tube, allowing a slight reduction of the anatomic dead space, which may be significant in situations when the V t is small.
However, this may sacrifice the ability to maintain a high P aw. Such an approach is often not possible in patients requiring HFOV. Suctioning patients on HFOV can be achieved using a closed inline system that does not require the patient to be disconnected from the oscillator.
The extent to which this prevents derecruitment is not clear.
In addition, a higher P aw may explain the reductions in cardiac preload that are occasionally seen with HFOV. Consequently, fluid balance needs to be carefully monitored as hypoxemia can, at times, be exacerbated by relative hypovolemia. Transportation out of the intensive care unit on the oscillator is currently not possible. Procedures like bronchoscopy may also lead to loss of P aw. Patients are switched back to conventional mechanical ventilation when they are able to tolerate a lower P aw currently 20—24 cmH 2 O.
However, the ideal timing is unknown and further work is required. Unlike in neonates, we know of no experience with transitioning adults directly to extubation from HFOV. The modest bias flow rates, which for the most part are insufficient to allow spontaneous respiratory efforts, are probably the primary reason that this has not occurred.
The use of HFOV has been extensively studied in the neonatal and pediatric populations.
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A number of studies did not show any significant benefit of HFOV over conventional ventilation in preventing chronic lung disease [ 34 - 37 ]. Two further studies have recently been released regarding HFOV in neonates, and are two of the largest to date in this field.
Johnson and colleagues randomized infants to HFOV versus conventional ventilation, and found no significant difference in mortality rates, chronic lung disease, or adverse events in the two groups [ 38 ]. In contrast, the study by Courtney and colleagues, which randomized a similar number of infants, found a significant benefit of HFOV over conventional ventilation in terms of earlier extubation and survival without oxygen therapy [ 39 ].
This study differed in that the infants were very high risk — g at birth and the ventilation protocols were more tightly controlled, suggesting that HFOV might be most useful if used in a uniform way in a well-defined population [ 40 ]. In contrast to the number of studies in neonates, where HFOV appears to have found a permanent home, evidence for HFOV in adults with lung injury is limited.
HFOV has until recently mostly been investigated as a rescue therapy for patients with ARDS who are failing conventional mechanical ventilation, because of difficulty in achieving either adequate ventilation or oxygenation within safe ventilator parameters.
Both studies suggested that mortality was improved in patients who had fewer pre-oscillator ventilator days. Although refractory hypoxemia can be problematic in managing patients with ARDS, multiple organ failure possibly exacerbated by biotrauma is often the cause of the patient's death [ 12 - 14 ].
A prospective, multicenter, randomized study has recently been published.