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Polysomnography tracings with neurally adjusted ventilatory assist (NAVA) and pressure support ventilation (PSV) in a representative subject. C4-A1 and O3-A2 are the electroencephalogram readings. ROC and LOC are the electrooculogram readings. Chin is the electromyogram reading. P peak is the peak airway 

Polysomnography tracings with neurally adjusted ventilatory assist (NAVA) and pressure support ventilation (PSV) in a representative subject. C4-A1 and O3-A2 are the electroencephalogram readings. ROC and LOC are the electrooculogram readings. Chin is the electromyogram reading. P peak is the peak airway 

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Objective: To compare the influence of 2 ventilation strategies on the occurrence of central apneas. Methods: This was a prospective, comparative, crossover study with 14 unsedated subjects undergoing weaning from mechanical ventilation in the medical ICU of Hôpital du Sacré-Cœur, Montréal, Québec, Canada. The subjects were ventilated alternatel...

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... a prospective, interventional, crossover study in a 22-bed medical ICU at H ˆpital du Sacr ́-Cœur over a 12-month period. Inclusion criteria were invasive mechanical ventilation, normal consciousness, absence of sedatives and opiates for Ն 24 h, and PSV with an F IO 2 below 0.60 and a PEEP of 5 cm H 2 O to achieve an S pO 2 of at least 90%. Exclusion criteria were presence of a central nervous system disorder, Glasgow Coma Scale score Ͻ 11, hemo- dynamic instability, renal and/or hepatic insufficiency, on- going sepsis, history of esophageal varices or gastroesoph- ageal bleeding in the past 30 days, and history of gastrointestinal symptoms such as vomiting. All subjects were ventilated through an endotracheal or tracheostomy tube. Subjects meeting the inclusion criteria were connected to a ventilator capable of delivering both PSV and NAVA (Servo-i, Maquet Critical Care, S ̈lna, Sweden). As previously described, 19 EAdi was recorded using a 16 French gastric catheter equipped with electrodes (EAdi catheter, Maquet Critical Care, S ̈lna, Sweden), whose correct position was checked using the “EAdi catheter positioning” ventilator function. Humidification was provided by a heat and moisture exchanger in all subjects. End-tidal CO 2 (P ETCO 2 ) was monitored with the Servo-i volumetric CO 2 module. PSV and NAVA were delivered in random order, determined using a closed-envelope technique. Each mode was delivered for 4 periods of 4 hours: 2 during the day (7:00 to 11:00 AM and 12:00 to 4:00 PM ) and 2 at night (10:00 PM to 2:00 AM and 3:00 to 7:00 AM ). To prevent possible data contamination from the previous mode of ventilation, data acquisition was delayed for 1 hour after each ventilator setting change (Fig. 1). Inspiratory pressure support was titrated to obtain a V T of 8 mL/kg of predicted body weight during active inspi- ration, without exceeding 20 cm H 2 O of pressure support and a breathing frequency of Ͻ 35 breaths/min. Flow- trigger sensitivity was set as low as possible (1–2 L/min) without inducing auto-triggering; cycling-off occurred when the inspiratory flow fell below 25% of the peak inspiratory flow. During PSV the ventilator function “NAVA Preview” was used to estimate the NAVA level required to achieve the same peak inspiratory pressure. After switching to NAVA, the settings were gradually adjusted to deliver the same assist level (peak pressure) and external PEEP as used previously with PSV. With NAVA the EAdi inspiratory trigger was at the lowest setting (0.5 ␮ V). EAdi was recorded with both ventilation modes and used to evaluate patient-ventilator synchrony. The backup apnea ventilation delay was set at 15 seconds, so that apneas lasting 10 seconds or more could be identified and their impact on sleep architecture (arousals) assessed. The electroencephalogram was recorded using standard electrode positions (left frontal/right auricular reference [F3/A2], right frontal/left auricular reference [F4-A1], left central/right auricular reference [C3/A2], right central/left auricular reference [C4/A1], left occipital/right auricular reference [O1/A2], and right occipital/left auricular reference [O2/A1] in the international 10 –20 system for electrode placement). 20 The standard reference was the left mastoid lead. 20 Two electrooculogram and 3 chin electromyogram leads were used to score rapid-eye-movement (REM) and non-REM sleep. The electroencephalogram, right and left electrooculograms, and submental electromyogram signals were amplified and recorded in the data acquisition system (Alice 5 polysomnography system using Alice Sleepware 2.5 software, Respironics, Murrys- ville, Pennsylvania). Sleep recordings were scored manually by a pulmo- nologist who was blinded to the study data and used Rechtschaffen and Kales criteria for sleep stages, 21 and American Sleep Disorder Association criteria for arousals and awakenings. 22,23 Central apneas were diagnosed ac- cording to international recommendations, 23 as absence of breathing and respiratory effort for at least 10 seconds (Fig. 2). Arousals and awakening were classified as apnea- related if they occurred within 3 breaths and/or 15 seconds of the end of an apnea. 24,25 Flow and pressure signals were acquired at a sampling rate of 100 Hz. Signals from each electrode pair were differentially amplified, digitized, and processed online, using previously described filters and algorithms. 26-28 Changes in diaphragm position along the array were accounted for using the cross-correlation technique, 29,30 and diaphragm-to-electrode distance filtering was minimized using the double-subtraction technique. 31 The root mean square was calculated for the subtracted signal and the signal obtained from the electrode pair on the diaphragm, and these values were summed every 16 ms to quantify EAdi. Signal segments with residual disturbances due to cardiac electric activity or common mode signals were identified using specific detectors and replaced by the previously accepted value. This processed EAdi signal was used to control the ventilator during NAVA and was si- multaneously acquired at a sampling rate of 2,000 Hz. EAdi was obtained from the ventilator through an RS232 interface, at a sampling rate of 100 Hz, and recorded using dedicated software (Nava Tracker 2.0, Maquet Critical Care, S ̈lna, Sweden). The input was analyzed using software (Analysis 1.0, Maquet Critical Care, S ̈lna, Sweden, and a customized version of Excel, Microsoft, Redmond, Washington). The peak of rectified and integrated EAdi swings (peak EAdi) was measured. From the flow signal we obtained the ventilator frequency (f-flow), flow-based inspiratory time, and flow-based expiratory time. To evaluate breathing pattern variability during the different sleep stages with each mode, we calculated the coefficient of variability (defined as the standard error/mean ratio ϫ 100) for V , breathing frequency, and peak EAdi. 32,33 The statistical analysis was performed using statistical software (SPSS 17.0, SPSS, Chicago, Illinois). Continuous variables are described as mean Ϯ SD. Data were compared using the general linear model for repeated measures. Given the small sample size, a nonparametric test was used to compare variables; we chose the Wilcoxon test for paired samples. Two-tailed P values smaller than .05 were considered significant. Variability data were compared using analysis of variance for repeated measures. We included 14 subjects, whose main characteristics at admission are reported in Table 1. Mechanical ventilation was required for acute respiratory failure in 10 subjects, postoperative cardiac complications in 3 subjects, and sep- tic shock in 1 subject. Mean PSV level was 15 Ϯ 5 cm H 2 O, and mean NAVA level was 1.6 Ϯ 1.4 cm H 2 O/ ␮ V. PEEP was kept at 5 cm H 2 O in all subjects with both ventilation modes. Mean total sleep time was 537 193 min. Mean sleep efficiency (the percentage of sleep during the study) was 56 20%. Table 2 reports the main breathing pattern data. Mean V ̇ E did not differ significantly between PSV and NAVA: 9.6 Ϯ 1.8 L/min and 9.3 Ϯ 1.8 L/min, respectively ( P ϭ .51). Mean breathing frequency was 17 Ϯ 4.6 breaths/min with PSV, and 18 Ϯ 5.7 breaths/min with NAVA ( P ϭ .14). The mean V ̇ E , V T , and breathing frequency did not differ significantly between the 2 ventilation modes. P ETCO 2 was not significantly different between the 2 modes during any of the sleep stages. V T differed significantly between the 2 ventilation modes during sleep stage 3– 4 (mean 391 Ϯ 57 mL with NAVA and 435 Ϯ 64 mL with PSV, P ϭ .005) and during REM sleep (mean 360 Ϯ 54 mL with NAVA and 415 Ϯ 61 mL with PSV, P ϭ .008, see Table 2). During PSV, V T did not vary significantly between wakefulness (429 Ϯ 65 mL) and REM sleep (415 Ϯ 61 mL) ( P ϭ .08). However, with NAVA, V T was significantly greater during wakefulness (419 Ϯ 63 mL) than during REM sleep (360 Ϯ 54 mL) ( P ϭ .001). V T differed significantly between stage 1 and REM sleep with both modes (NAVA 431 Ϯ 69 mL vs 360 Ϯ 54 mL, respectively, P ϭ .001, PSV 442 Ϯ 61 mL vs 415 Ϯ 61 mL, respectively, P ϭ .001, see Table 2). Mean breathing frequency during non-REM sleep did not differ significantly between the 2 ventilation modes. During REM sleep, in contrast, mean breathing frequency was significantly higher with NAVA than with PSV (15 Ϯ 3 breaths/min and 13 Ϯ 2 breaths/min, respectively, P ϭ .004). During wakefulness the mean breathing frequency was also significantly higher with NAVA (20 Ϯ 4 breaths/min and 18 Ϯ 3 breaths/min, respectively, P ϭ .005, see Table 2). Table 3 shows the oscillatory behavior of V T , breathing frequency, V ̇ E , and P ETCO 2 during sleep stages 2 and 3– 4 with PSV. Sleep apnea occurred in 10 subjects, all of whom had either COPD or chronic heart failure, 2 known risk factors for central apneas. Moreover, these subjects experienced hyperventilation during sleep, which preceded the central apneas. Table 3 reports the mean number of sleep apneas per hour of sleep in the ...

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... These patients should be considered better candidates for another type of ventilatory support. However, it is interesting to note that some studies in adults have shown that during IMV weaning, "overassistance" apneas are less frequent with NAVA compared with pressure-support ventilation [30]. ...
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... In contrast to monotonous ventilation delivered by more conventional ventilatory modes, such as pressure-controlled ventilation www.frontiersin.org (PCV), pressure support ventilation (PSV), or volume-controlled ventilation (VCV), the variability of pressure and tidal volume is higher during NAVA (11,(22)(23)(24). NAVA permits to transmit the variability of the respiratory center demand into pressure (and volume) variability (11,22,23). ...
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... The intra-individual temporal NRR variability was also quantified using coefficients of variation of NRR, which were affected by the ventilatory condition (p < 0.01, Figure 3B). While the variability of NRR was low in the control group (CV 22% [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28]) and during NAVA (28% , p = 0.33 vs. control), the CVs were 42% during PSV (p = 0.09 vs. control), and 63% during PCV (p = 0.02 vs. control). ...
... 6,8 Delisle et al, in this issue of RESPIRATORY CARE, report results of their study examining any association between the occurrence of central apneas during weaning and the application of NAVA or pressure support ventilation. 9 NAVA triggering was applied when the EAdi reached 0.5 V, and the EAdi signal was measured every 16 ms, both of which are consistent with the application of NAVA in other literature. 6,8 Delisle et al have identified a statistically significant increase in tidal volume variability when supported breaths were flow assisted by NAVA, a finding that is consistent with the conclusions of other recent publications. ...
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... The absence of desaturation during neural apneas is likely attributable to the backup ventilatory rate. The lack of neural apneas during NAVA is consistent with previous studies on adult patients [21] . Interpreting this finding, however, is not easy at all. ...
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Objective: To compare neurally adjusted ventilatory assist and conventional ventilation on patient-ventilator interaction and neural breathing patterns, with a focus on central apnea in preterm infants. Design: Prospective, observational cross-over study of intubated and ventilated newborns. Data were collected while infants were successively ventilated with three different ventilator conditions (30 min each period): 1) synchronized intermittent mandatory ventilation (SIMV) combined with pressure support at the clinically prescribed, SIMV with baseline settings (SIMVBL), 2) neurally adjusted ventilatory assist, 3) same as SIMVBL, but with an adjustment of the inspiratory time of the mandatory breaths (SIMV with adjusted settings [SIMVADJ]) using feedback from the electrical activity of the diaphragm). Setting: Regional perinatal center neonatal ICU. Patients: Neonates admitted in the neonatal ICU requiring invasive mechanical ventilation. Measurements and main results: Twenty-three infants were studied, with median (range) gestational age at birth 27 weeks (24-41 wk), birth weight 780 g (490-3,610 g), and 7 days old (1-87 d old). Patient ventilator asynchrony, as quantified by the NeuroSync index, was lower during neurally adjusted ventilatory assist (18.3% ± 6.3%) compared with SIMVBL (46.5% ±11.7%; p < 0.05) and SIMVADJ (45.8% ± 9.4%; p < 0.05). There were no significant differences in neural breathing parameters, or vital signs, except for the end-expiratory electrical activity of the diaphragm, which was lower during neurally adjusted ventilatory assist. Central apnea, defined as a flat electrical activity of the diaphragm more than 5 seconds, was significantly reduced during neurally adjusted ventilatory assist compared with both SIMV periods. These results were comparable for term and preterm infants. Conclusions: Patient-ventilator interaction appears to be improved with neurally adjusted ventilatory assist. Analysis of the neural breathing pattern revealed a reduction in central apnea during neurally adjusted ventilatory assist use.
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Compared with the conventional forms of partial support, neurally adjusted ventilatory assist was repeatedly shown to improve patient-ventilator synchrony and reduce the risk of overassistance, while guaranteeing adequate inspiratory effort and gas exchange. A few animal studies also suggested the potential of neurally adjusted ventilatory assist in averting the risk of ventilator-induced lung injury. Recent work adds new information on the physiological effects of neurally adjusted ventilatory assist. Compared with pressure support, neurally adjusted ventilatory assist has been shown to improve patient-ventilator interaction and synchrony in patients with the most challenging respiratory system mechanics, such as very low compliance consequent to severe acute respiratory distress syndrome and high resistance and air trapping due to chronic airflow obstruction; enhance redistribution of the ventilation in the dependent lung regions; avert the risk of patient-ventilator asynchrony due to sedation; avoid central apneas; limit the risk of high (injurious) tidal volumes in patients with acute respiratory distress syndrome of varied severity; and improve patient-ventilator interaction and synchrony during noninvasive ventilation, irrespective of the interface utilized. Several studies nowadays prove the physiological benefits of neurally adjusted ventilatory assist, as opposed to the conventional modes of partial support. Whether these advantages translate into improvement of clinical outcomes remains to be determined.