Objective. To assess volume guarantee (VG) ventilation combined with high-frequency oscillatory ventilation (HFOV) strategy on PaCO2 regulation in an experimental model of neonatal distress syndrome. Methods. Six 2-day-old piglets weighing ？kg were used for this interventional experimental study. Animals were ventilated during physiologic lung conditions and after depletion of lung surfactant by bronchoalveolar lavage (BAL). The effect of HFOV combined with VG on PaCO2 was evaluated at different high-frequency expired tidal volume (VThf) at constant frequency ( ) and mean airway pressure (mPaw). Fluctuations of the pressure (ΔPhf) around the mPaw and PaCO2 were analyzed before and after lung surfactant depletion. Results. PaCO2 levels were inversely proportional to VThf. In the physiological lung condition, an increase in VThf caused a significant decrease in PaCO2 and an increase in ΔPhf. After BAL, PaCO2 did not change as compared with pre-BAL situation as the VThf remained constant by the ventilator. Conclusions. In this animal model, using HFOV combined with VG, changes in the VThf settings induced significant modifications in PaCO2. After changing the lung condition by depletion of surfactant, PaCO2 remained unchanged, as the VThf setting was maintained constant by modifications in the ΔPhf done by the ventilator. 1. Introduction High-frequency oscillatory ventilation (HFOV) is characterized by an effective gas exchange using tidal volumes equal to or less than the dead space volume [1] at supraphysiological frequencies. Carbon dioxide (CO2) removal is mostly related to the tidal volume generated during high-frequency ventilation [2–5], and this high-frequency expired tidal volume (VThf) is known to be close to the airway dead space [6]. Also, the frequency ( ) has a role in CO2 removal [7] and has an independent effect on the distribution of the gas within the airways [8]. During HFOV, several mechanisms of gas exchange have been described, the combination of which is responsible for its ventilatory efficiency [9]. As HFOV uses a tidal volume lower or equal to the anatomical dead space, it has been argued that the incidence of bronchopulmonary dysplasia (BPD) can be reduced [10]. Although other potential mechanisms have been described by which HFOV causes less ventilator-induced lung damage [11], the prevalence of BPD in preterm infants treated with HFOV is similar to those undergoing conventional ventilation [12]. VThf is crucial for CO2 elimination and has a larger impact on CO2 removal during HFOV in comparison to tidal volume during
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