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 2.57 ± 0.26 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 (f R) 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.
Previous research has demonstrated the potential benefit derived from the combination of high frequency oscillatory ventilation and volume guarantee mode (HFOV‐VG), a procedure that allows us to explore and control very low tidal volumes. We hypothesized that secondary spontaneous change in oscillation pressure amplitude (∆Phf), while increasing the mean airway pressure (MAP) using HFOV‐VG can target the lung recruitment. Methods A two‐step animal distress model study was designed; in the first‐step (ex vivo model), the animal's lungs were isolated to visually check lung recruitment and, in the second one (in vivo model), they were checked through arterial oxygen partial pressure improvement. Baseline measurements were performed, ventilation was set for 10 min and followed by bronchoalveolar lavage with isotonic saline to induce depletion of surfactant and thereby achieve a low compliance lung model. The high‐frequency tidal volume and frequency remained constant and the MAP was increased by 2 cmH2O (ex vivo) and 3 cmH2O steps (in vivo) every 2 min. Changes in ΔPhf to achieve the fixed volume were recorded at the end of each interval to describe the maximum drop point as the recruitment point. Results Fourteen Wistar Han rats were included, seven on each sub‐study described. After gradual MAP increments, a progressive decrease in ΔPhf related to recruited lung regions was visually demonstrated. In the in vivo model we detected a significant comparative decrease of ΔPhf, when measured against the previous value, after reaching a MAP of 11 cmH2O up to 17 cmH2O, correlating with a significant improvement in oxygenation. Conclusion The changes in ∆Phf, linked to a progressive increase in MAP during HFOV‐VG, might identify optimal lung recruitment and could potentially be used as an additional lung recruitment marker.
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