High-frequency percussive ventilation.

In the June 2010 issue of the Journal, Allan concluded from an in vitro study of high-frequency percussive ventilation (HFPV) that this ventilation mode may deliver injurious tidal volumes (VT). Allan claimed that the results from his experiments showed that with a commercially available Fleisch-type pneumotachograph (3700, Hans Rudolph, Shawnee, Kansas) he was able to measure the mean VT of the highfrequency breaths and the low-frequency breaths delivered by HFPV. Allan’s objective was to validate a pneumotachograph for HFPV and then exploit data to describe the behavior of both the high and low frequency breaths. Lucangelo et al, in 2004, conducted a similar study of HFPV and published their data on mean airway pressure measurements, peak inspiratory pressure, positive peak flow, negative peak flow, and VT in a lung model, using different levels of compliance and resistance.2 In Lucangelo’s experiment, VT measurements were obtained by digitally integrating the flow signals of the high and low frequency breaths. Inspiratory positive and negative peak flows were measured during pulse breaths to determine the highest and lowest positive and negative values for the pulse flows characteristic of HFPV. A lung simulator (Medishield, Harlow Essex, United Kingdom) was used and set at 15 different elastic and resistive load combinations. Flow was measured with a number 2 Fleisch-like pneumotachograph connected to a differential pressure transducer positioned between the HFPV device and the lung simulator. The high-frequency rate was 500 breaths/min, the phase (conventional) rate was 10 breaths/min, and the inspiratory-expiratory ratio was 1:1.25. Using different combinations of compliance and resistance settings, measurements of peak airway pressure, mean airway pressure, inspiratory positive peak flow, inspiratory negative peak flow, and VT were collected and fed to an analog-to-digital converter. Measured VT ranged between 115 mL and 465 mL, using up to 45.43 cm H2O of peak pressure, with various combinations of resistance and compliance settings on the test lung. The smallest VT measured was associated with the highest impedance values of compliance and resistance. Lucangelo et al concluded that under similar clinical conditions, since VT delivered decreased with a decrease in lung compliance, this could be interpreted as a lung-protective mechanism in HFPV. As pointed out by Lucangelo et al, the gas flow characteristics of HFPV are unique in that the small percussive sub-tidal volumes have both positive and negative “minibursts,” which cause gas wash-out that is thought to account for the smaller VT actually delivered to the patient connection. The venturi system within the HFPV device portion of the ventilator circuit will reduce entrainment of gases as intrapulmonary pressures increase, which was demonstrated by the fall in inspiratory flowin that experiment. Lucangelo et al concluded that HFPV creates a minimum amount of generated volume, even under maximum implied load conditions. The absolute values of the positive and negative peak flows with the delivered high-frequency breaths net a flow that nearly equals zero. Although the highfrequency breaths are useful for gas exchange, Lucangelo et al identified that they do not add significantly to the VT delivered to the patient. Lucangelo differentiated between VT that the lung actually experiences with HFPV by subtracting measured actual volume expired from actual VT delivered with an inspiratory breath. Allardet-Servent et al, in 2008, tested HFPV in a prospective randomized controlled in vivo animal study.3 Forty-three rabbits were subjected to lung injury by intratracheal instillation of human gastric juices, and randomized to HFPV, low-VT (6 mL/kg) mechanical ventilation, high-frequency-oscillation ventilation (HFOV), or high-VT (12 mL/kg) mechanical ventilation. The group found that, like HFOV and low-VT ventilation, HFPV provided lung protection while improving oxygenation and ventilation. The animals treated with HFPV showed dramatically less damage to lung tissue macroscopically and via microphotography, similar to the HFOV and low-VT ventilated treatment groups. The lung-injury scores in the HFPV group were similar to those in the HFOV and low-VT groups. Allardet-Servent postulated that with HFPV, like HFOV, there is a considerable drop in airway pressure between the trachea and the alveoli, and HFPV is therefore considered an effective lung-protective strategy. Bougatef et al in, November 2007, reported on 15 years of experience using HFPV in premature infants, and described the successful management of respiratory distress syndrome with HFPV in a retrospective study that compared HFPV to conventional ventilation.4 The infants included in that study were initially managed with an average peak inspiratory pressure of 25 cm H2O, PEEP of 6 cm H2O, a conventional rate of 40 breaths/min, and high-frequency rate of 600–900 breaths/min. There were lower incidences of chronic lung disease, pulmonary air leak, and elevated intracranial pressure in the HFPV group than in the conventionally ventilated group. Bougatef et al have been using HFPV in their neonatal intensive care unit since 1985, and they consider HFPV a lung-protective strategy for the smallest babies treated at their institution. Mlcak et al, in 2002, compared HFPV and conventional ventilation in 86 pediatric patients with inhalation injury.5 Forty-three patients were randomized to conventional ventilation and 43 to HFPV. Mlcak et al concluded that HFPV can significantly reduce delivered peak pressure, making HFPV an ideal protective ventilation strategy, especially in lungs that have been damaged by inhalation injury. Reyburn et al, in 2008, compared noninvasive HFPV via nasal cannula to pressure-control intermittent mandatory ventilation (PC-IMV) in preterm lambs. Both groups were managed for 3 days.6 Reyburn et al found that oxygenation and ventilation targets were sustained with lower airway pressure in the HFPV group than in the PCIMV group. Notably, the HFPV group had less thinning of alveolar walls and more apoptosis and less proliferation among mesenchymal cells than the PC-IMV group. They concluded that HFPV via nasal cannula preserved the balance between mesenchymal cell apoptosis and proliferation in the distal air-spaces, so that alveolarization progresses in a natural fashion. Lung growth appeared to proceed during the 3-day ob-