Eighty three percent of the subjects were exposed to maternal steroids and 96% received postnatal surfactant. Average gestational age was 26.5 ± 2.3 weeks (range 24 weeks to 33 weeks) and their average age at the time of data collection was 8 ± 9 days (range 1 to 36 days). The subjects weighed 862 ± 361 g (range 500 to 2040 g) at the time of data collection. Circuit compliance was turned off on one subject, leaving only twenty-six subjects with reportable tidal volume data. Twenty-seven subjects underwent data collection for PIP and VT on invasive NAVA. Unless otherwise noted, all testing was two-tailed and evaluated at the type I error rate of alpha = 0.05 level of statistical significance. Statistical analyses were completed using SAS 9.4/14.2©. The chi-square test of independence was used to assess the relationship between group and NAVA level, followed by the chi-square test for trend to assess for evidence of trends of VT and PIP by NAVA level in both the NAVA and NIV-NAVA groups. The χ 2 Mantel-Haenszel Trend Test was used to assess and describe the potential relationships of NAVA levels with group, PIP (quartiles), and VT (quartiles). Post hoc pairwise testing with Tukey adjustments was done to control for type I error rate. A factorial ANOVA was conducted to assess for potential differences in PIP by main effects of group and NAVA level as well as their interaction. The independent samples t test was conducted to assess for potential difference in overall PIP by group (NIV-NAVA vs. Data were recorded separately for each variable without time stamps and subjects had variable numbers of observations for P-Peak and VT therefore, the P-Peak values and the VT values could not be linked by observation. Based on clinical rationale, each observation is viewed as independent therefore, the statistical analysis was conducted on the full set of observations. We therefore planned to evaluate the range of PIP and VT that premature neonates generate while on NAVA.Įxamination of data included calculation of summary statistics for continuous data, along with frequencies and percentages for categorical data. Despite NAVA’s neuro-ventilatory coupling advantage that NAVA ventilation provides, concern has been raised that enabling premature neonates to choose their own ventilator parameters could result in excessively high PIPs and VTs, theoretically increasing the risk of pneumothorax acutely, and chronic lung disease over the long term. By optimally supporting native breathing reflexes, NAVA can facilitate patient effort in a synchronous fashion. Studies have shown that neonates, while in both invasive and non-invasive NAVA, have the ability to “switch-off” neural inspiration, and then cycle-off the ventilator when an appropriate volume/pressure has been reached. When properly positioned, it can accurately and reliably trigger and cycle the ventilator breath, independent of airway leaks, making it ideal for synchronizing non-invasive ventilation. This Edi signal is obtained from a specialized indwelling nasogastric feeding tube with embedded sensing electrodes (NAVA catheter). The patient controls the amount of pressure delivered by the ventilator using the electrical activity of the diaphragm (Edi) waveform to trigger-on and cycle-off each assisted breath, therefore providing truly synchronized ventilation. Neurally adjusted ventilatory assist (NAVA) ventilation allows patients to control their own peak inspiratory pressure (PIP) and VT on a breath-to-breath basis. Typical VT ranges to initiate tidal volume ventilation (VTV) range from 4 to 7 ml/kg. Data for selecting the appropriate target tidal volume (VT) for specific patients with different clinical conditions are limited. When compared to pressure-limited ventilation, the use of volume-targeted ventilation has been associated with more favorable outcomes. Despite advancements in neonatal ventilation modalities, premature neonates remain at significant risk for bronchopulmonary dysplasia (BPD).
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