Neurally adjusted ventilatory assist can improve arterial oxygenation
Details
Serval ID
serval:BIB_7F1B89647AB8
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Abstract (Abstract): shot summary in a article that contain essentials elements presented during a scientific conference, lecture or from a poster.
Collection
Publications
Institution
Title
Neurally adjusted ventilatory assist can improve arterial oxygenation
Title of the conference
23rd Annual Meeting of the European Society of Intensive Care Medicine
Address
Barcelona, Spain, October 9-13, 2010
Publication state
Published
Issued date
2010
Volume
36
Series
Intensive Care Medicine
Pages
S326
Language
english
Notes
Meeting Abstract
Abstract
INTRODUCTION. Neurally Adjusted Ventilatory Assist (NAVA) [1] is a new spontaneousassisted ventilatory mode which uses the diaphragmatic electrical activity (Eadi) to pilot the ventilator. Eadi is used to initiate the ventilator's pressurization and cycling off. Delivered inspiratory assistance is proportional to Eadi. NAVA can improve patient-ventilator synchrony [2] compared to pressure support (PS), but little is known about its effect on minute ventilation and oxygenation.
OBJECTIVES. To compare the effects of NAVA and PS on minute ventilation and oxygenation and to analyze potential determinant factors for oxygenation.
METHODS. Comparison between two 20-min periods under NAVA and PS. NAVA gain (proportionality factor between Eadi and delivered pressure) set as to obtain the same peak pressure as in PS. FIO2 and positive end-expiratory pressure (PEEP) were the same in NAVA and PS. Blood gas analyses were performed at the end of both recording periods. Statistical analysis: groups were compared with paired t tests or non parametric Wilcoxon signed-rank tests. p\0.05 was considered significant.
RESULTS. [Mean ± SD]: 22 patients (age 66 ± 12 year, 7 M/15F, BMI 23.4 ± 3.1 kg/m2), 8 patients with COPD. Initial settings: PS 13 ± 3 cmH2O, PEEP 7 ± 2 cmH2O, NAVA gain 2.2 ± 1.8. Minute ventilation and PaCO2 were the same with both modes (p = 0.296 and 0.848, respectively). Tidal volume was lower with NAVA (427 ± 102 vs. 477 ± 102 ml, p\0.001). In contrast respiratory rate was higher with NAVA (25.6 ± 9.5 vs. 22.3 ± 8.9 cycles/min). Arterial oxygenation was improved with NAVA (PaO2 85.1 ± 28.9 vs. 75.8 ± 11.9 mmHg, p = 0.017, PaO2/FIO2 210 ± 53 vs. 195 ± 58 mmHg, p = 0.019). Neural inspiratory time (Tin) was comparable between NAVA and PS (p = 0.566). Among potential determinant factors for oxygenation, mean airway pressure (Pmean) was lower with NAVA (10.6 ± 2.6 vs. 11.1 ± 2.4 cmH2O, p = 0.006), as was the pressure time product (PTP) (6.8 ± 3.0 vs. 9.2 ± 3.5 cmH2O 9 s, p = 0.004). There were less asynchrony events with NAVA (2.3 ± 2.0 vs. 4.4 ± 3.8, p = 0.009).Tidal volume variability was higher with NAVA (variation coefficient: 30 ± 19.5 vs. 13.5 ± 8.6, p\0.001). Inspiratory time in excess (Tiex) was lower with NAVA (56 ± 23 vs. 202 ± 200 ms, p = 0.001).
CONCLUSION. Despite lower Pmean and PTP in NAVA, arterial oxygenation was improved compared to PS. As asynchronies may be associated with an increased work of breathing and a higher oxygen consumption, their decrease in number with NAVA could be an explanation for oxygenation improvement. Another explanation could be the increase in VT variability. Further studies should now be performed to confirm the potential of NAVA in improving arterial oxygenation and explore the underlying mechanisms.
OBJECTIVES. To compare the effects of NAVA and PS on minute ventilation and oxygenation and to analyze potential determinant factors for oxygenation.
METHODS. Comparison between two 20-min periods under NAVA and PS. NAVA gain (proportionality factor between Eadi and delivered pressure) set as to obtain the same peak pressure as in PS. FIO2 and positive end-expiratory pressure (PEEP) were the same in NAVA and PS. Blood gas analyses were performed at the end of both recording periods. Statistical analysis: groups were compared with paired t tests or non parametric Wilcoxon signed-rank tests. p\0.05 was considered significant.
RESULTS. [Mean ± SD]: 22 patients (age 66 ± 12 year, 7 M/15F, BMI 23.4 ± 3.1 kg/m2), 8 patients with COPD. Initial settings: PS 13 ± 3 cmH2O, PEEP 7 ± 2 cmH2O, NAVA gain 2.2 ± 1.8. Minute ventilation and PaCO2 were the same with both modes (p = 0.296 and 0.848, respectively). Tidal volume was lower with NAVA (427 ± 102 vs. 477 ± 102 ml, p\0.001). In contrast respiratory rate was higher with NAVA (25.6 ± 9.5 vs. 22.3 ± 8.9 cycles/min). Arterial oxygenation was improved with NAVA (PaO2 85.1 ± 28.9 vs. 75.8 ± 11.9 mmHg, p = 0.017, PaO2/FIO2 210 ± 53 vs. 195 ± 58 mmHg, p = 0.019). Neural inspiratory time (Tin) was comparable between NAVA and PS (p = 0.566). Among potential determinant factors for oxygenation, mean airway pressure (Pmean) was lower with NAVA (10.6 ± 2.6 vs. 11.1 ± 2.4 cmH2O, p = 0.006), as was the pressure time product (PTP) (6.8 ± 3.0 vs. 9.2 ± 3.5 cmH2O 9 s, p = 0.004). There were less asynchrony events with NAVA (2.3 ± 2.0 vs. 4.4 ± 3.8, p = 0.009).Tidal volume variability was higher with NAVA (variation coefficient: 30 ± 19.5 vs. 13.5 ± 8.6, p\0.001). Inspiratory time in excess (Tiex) was lower with NAVA (56 ± 23 vs. 202 ± 200 ms, p = 0.001).
CONCLUSION. Despite lower Pmean and PTP in NAVA, arterial oxygenation was improved compared to PS. As asynchronies may be associated with an increased work of breathing and a higher oxygen consumption, their decrease in number with NAVA could be an explanation for oxygenation improvement. Another explanation could be the increase in VT variability. Further studies should now be performed to confirm the potential of NAVA in improving arterial oxygenation and explore the underlying mechanisms.
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Create date
11/11/2010 15:58
Last modification date
11/10/2019 20:06