# Neurally adjusted ventilatory assist in critical care patients with and without obesity: a prospective randomized crossover study

Matthieu Conseil, Samir Jaber, Fabrice Galia, Nicolas Molinari, Gerald Chanques, Audrey de Jong, Mathieu Capdevila

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Matthieu Conseil, Samir Jaber, Fabrice Galia, Nicolas Molinari, Gerald Chanques, et al.. Neurally adjusted ventilatory assist in critical care patients with and without obesity: a prospective randomized crossover study. Annals of Intensive Care, 2025, 15 (128), pp.11. 10.1186/s13613-025-01552-x. hal-05229333v2

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# Neurally adjusted ventilatory assist in critical care patients with and without obesity: a prospective randomized crossover study

Matthieu Conseil¹,², Samir Jaber¹,²*, Fabrice Galia¹, Nicolas Molinari³, Gerald Chanques¹,², Audrey De Jong¹,² and Mathieu Capdevila¹,²

**Abstract**

**Background** Neurally Adjusted Ventilatory Assist (NAVA) compared to Pressure Support Ventilation (PSV) improves patient-ventilator interactions in intensive care unit. No study has evaluated NAVA in patients with obesity. We aimed to assess the feasibility and safety of NAVA in patients with obesity, and to compare NAVA in patients with versus without obesity.

**Methods** In this randomized cross-over study, all respiratory cycles during 1 h of mechanical ventilation from 10 patients with obesity and 11 without obesity were analyzed. Patients underwent 30 min of NAVA and 30 min of PSV in a random order. Flow, airway pressure and diaphragm electrical activity were continuously recorded. Arterial blood gases were obtained at baseline and at the end of each 30-min period. Patient-ventilator interactions were assessed with trigger delay, inspiratory time in excess, rate and type of dyssynchrony cycles. Variability of the ventilatory parameters was evaluated by the coefficient of variation (SD/mean).

**Results** All patients concluded the study, with a total of 1790 ± 873 respiratory cycles analyzed per patient. In patients with obesity, NAVA versus PSV was associated with a significant reduction in trigger delay (0 [0–5] vs. 106 [34–125] ms, *p* < 0.05), inspiratory time in excess (96 [94–102] vs. 145 [137–202] ms, *p* < 0.01) and in ineffective efforts (0 [0-0.03] vs. 0.33 [0.23–0.37] events/min, *p* < 0.05). The global dyssynchrony index remained similar in both modes (2.2% [1.1–4.4] vs. 3.7% [2.4–5.6], *p* = 0.68). Compared to PSV, PaO2/FiO2 ratio significantly increased in NAVA, 238 mmHg [174–344] versus 207 mmHg [164–297], *p* < 0.05. The tidal volume was significantly lower during NAVA than during PSV, 6.7 mL/kg predicted body weight [5.9–7.1] versus 7.2 mL/kg [6.2–8.2], *p* < 0.05. Ventilatory variability was significantly higher with NAVA, 16% [11-21] versus 4% [2-4] in mean inspiratory airway pressure. These results were similar in patients without obesity and the obesity factor was never significant. No adverse event was observed in patients with and without obesity in both modes.

**Conclusion** In patients with obesity, NAVA ventilation is feasible and safe, improves patient-ventilator interactions and oxygenation, with an increase ventilatory variability compared to PSV. The effects of NAVA are comparable in patients with and without obesity.

Full list of author information is available at the end of the article

<figure><img src="image_3.png" /></figure>

<footnote>*Correspondence:
Samir Jaber
s-jaber@chu-montpellier.fr</footnote>
**Keywords** Nava, Obesity, Weaning, Mechanical ventilation

**Introduction**

Pressure Support Ventilation (PSV) is the most used mode during the weaning of mechanical ventilation in intensive care unit [1, 2]. However the patient's ventilatory demand is variable and this mode provides a fixed level of pressure, which may lead to a mismatch between the patient's request and the level of assistance. Neutrally Adjusted Ventilatory Assist (NAVA) is a mode of mechanical ventilation where the diaphragm electrical activity (EADi) controls the timing and the amount of assistance [3]. In critically ill patients NAVA can improve patient-ventilator synchrony [4, 5, 6], respiratory variability [7, 8], oxygenation [8], and it can decrease the duration of mechanical ventilation [9]. In situation of difficult weaning, NAVA could be a more appropriate mode than PSV [10]. These benefits were also confirmed with non-invasive ventilation, in chronic obstructive pulmonary disease exacerbation [11], during acute respiratory failure [12] and after extubation [13].

Over the past years, there has been a significant increase in obesity rates worldwide [14] and the prevalence of patient with obesity is increasing in intensive care units [15, 16]. Patients with obesity have impaired lung function with decreased functional residual capacity and compliance, increased airway resistance and ventilation-perfusion mismatch [17]. These changes are causing an increased incidence of complications and a longer duration of weaning from mechanical ventilation in intensive care [17]. Specific respiratory management is required during weaning and after extubation for these patients [18, 19, 20].

However, diaphragmatic electromyogram (EMG) acquisition, necessary for NAVA, could be compromised by increased fatty infiltration of the respiratory muscles and pleura [21, 22]. Signal acquisition could also be affected by the distance between diaphragm and esophagus [23] related to obesity. To our knowledge no physiological study has been performed to evaluate the use of NAVA in patients with obesity.

The hypothesis of the present study is that NAVA use is feasible and safe in patients with obesity.

The first objective of this study was to evaluate the safety and the effectiveness (ventilator parameters, gas exchange and dyssynchronies) of NAVA in patients with obesity. The secondary objective was to compare NAVA in patients with and without obesity.

**Materials and methods**

This randomized cross-over study was conducted in a single center of Montpellier University Hospital. The institutional review board (Comité de Protection des

Personnes Sud Méditérannée IV, Montpellier, France) approved the protocol (ref number: 2009-A00087-50). Written informed consent was provided by the patient or surrogates.

**Patients**

All consecutive patients with obesity (defined as Body Mass Index (BMI) $\ge$ 30 kg/m$^2$) and without obesity (BMI < 30 kg/m$^2$) under invasive mechanical ventilation for at least 24 h were evaluated for inclusion in the study. Patients mechanically ventilated via an endotracheal tube for more than 24 h and ventilated in PSV were included if they have the following inclusion criteria: patient alert and calm corresponding to a Richmond Agitation Sedation Scale (RASS) between -3 and 0, inspired oxygen inspired fraction ($FiO_2$)$\le$60% with positive end-expiratory pressure (PEEP)$\le$10 cm H$_2$O. Patients were affiliated to the social security system.

The exclusion criteria were age < 18 years, pregnancy, contraindications for an EADi catheter placement, clinical instability for any reason and decision to withhold life-sustaining treatment. Without being completely excluded from the study, some patients may be excluded from secondary analyses due to a lack of data or technical issues.

Patients with obesity were divided into three groups based on BMI for subgroup analysis.

**Ventilator**

All the patients included were ventilated using a Servo-I (Maquet Critical Care AB ®, Solna, Sweden) equipped with the standard version of the NAVA module. In PSV the assistance was triggered and cycled off by the flow signal and the amount of assistance (pressure support level) is fixed. In NAVA the assistance can be triggered by the EADi signal or by flow signal and the amount of assistance is proportional to electrical activity of the diaphragm (the proportionality factor is set by the physician) [3]. EADi was obtained with a specific nasogastric tube which has ten electrodes at its distal (EADi catheter; Maquet Critical Care, Sölna, Sweden).

**Protocol**

After inclusion, the nasogastric tube was replaced by the EADi catheter positioned according to the manufacturer's recommendations. Each patient was placed in a semi-recumbent position and consecutively ventilated for 30 min with PSV mode and NAVA mode in random order.

In both modes the levels of inspired oxygen fraction ($FiO_2$) and positive end-expiratory pressure (PEEP)
were the same as those set before inclusion according to usual practice of the center (FiO₂ for SpO₂ > 92% and PEEP between 5 and 10 cmH₂O). The pressure support level and the NAVA level were adjusted by the investigator to obtain a tidal volume (VT) between 6 and 8 ml/kg predicted body weight (PBW) [8]. In the PSV mode flow inspiratory trigger was set to its lowest value without cause autotrigging and cycled off occurred when the inspiratory flow decreased at 30% of its peak inspiratory flow value. In the NAVA mode, neural inspiratory trigger was set at 0.5µV and neural expiratory trigger was set at 70% of peak EADi value. Once ventilator settings realized they were no longer modified during the study period.

## Measurements

Respiratory parameters (airway pressure, flow and EADi) were acquired at 50 Hz from the ventilator via a RS232 cable connected to a computer using commercially available software (Servo-I RCR, version 3.6, Maquet Critical Care) at each mode for 30 min after 5 min of stabilization (Figure S1).

RASS, Behavioral Pain Scale (BPS) and hemodynamics variables (blood pressure and heart rate) were obtained at the beginning and at the end of each mode.

Arterial blood gases were collected at the inclusion and at the end of each mode in patients equipped with an arterial catheter. Respiratory rate (RR), Inspiratory time (Ti), Total respiratory time (Ttot), Tidal Volume (VT), VT/kg (PBW), Minute Ventilation (MV) were obtained from flow recordings; Maximal (Max P<sub>insp</sub>) and mean inspiratory airway pressure (Mean P<sub>insp</sub>) were obtained from airway pressure and maximal EADi from EADi signal. The inspiratory trigger delay (T<sub>d</sub>) was calculated as the time lag between the beginning of EADi swing and the beginning of ventilator inspiratory flow. The inspiratory time in excess (T<sub>iex</sub>, in ms) was calculated as the time lag between the ventilator inspiratory pressurization time and the neural inspiratory time.

The numbers of five types of patient-ventilator dys synchrony (Ineffective efforts, Auto-triggering, Premature cycling, Delayed cycling, and Double triggering) per minute were determined by the investigator and described in supplemental digital content. In NAVA, double triggering were differentiated into 2 groups: type 1 which was caused by a biphasic EADi signal and type 2 when the cause was different in both modes. Dyssynchronies detection was based on visual inspection of flow, airway pressure and EADi signal. We calculated the Dyssynchrony index (DI) expressed in percentage (dys synchronous events over the sum of ventilator cycles and ineffective efforts) as previously published [8].

## Statistical analysis

To validate the feasibility of NAVA in patients with obesity, we planned to include up to 10 analyzable patients with obesity, using a convenience sample based on previous studies [8, 12]. We then planned to include up to 10 analyzable patients without obesity to compare the physiological benefits of NAVA between obese and non-obese patients as exploratory outcomes. Data are expressed as median [interquartile range] or mean ± SD according to the type of variable distribution. Kolmogorov-Smirnov test was used to assess normal distribution of data. Comparisons between NAVA and PSV in same patients were performed using paired Student's t-test or Wilcoxon test according to the data distribution. Comparisons between patients with obesity and patients without obesity were performed using Student's t-test or Mann Whitney test according to the data distribution. The level of significance was *p* < 0.05.

We evaluated the variability of each ventilatory variables (RR, Ti, Ttot, VT, VM, Max Pinsp, Mean Pinsp, Max EADi) by the coefficients of variation expressed in percentage (standard deviation multiplied by 100 and divided by the mean) as described previously [24].

Linear regression analysis was performed between VT/kg and Max P<sub>insp</sub>.

The statistical analysis was performed using the software MedCalc® (MedCalc Software, Broekstraat, Belgium).

## Results

Ten patients with obesity with a BMI of 35 [31, 32, 33, 34, 35, 36, 37, 38] and 12 without obesity with a BMI at 26 [25, 26, 27, 28] (*p* < 0.01) were included in the study. One patient without obesity was excluded because of the absence of EADi signal (diagnosis of amyotrophic lateral sclerosis), thus 21 patients were analyzed (Figure S2) with a total of 1790 ± 873 respiratory cycles analyzed per patient. Admission pathology in Intensive Care Unit (ICU) and clinical characteristics of the 21 patients who concluded the study are summarized in Table 1. No patients had medical history of chronic obstructive pulmonary disease and none was tracheotomized. Arterial blood gases were available for 18 patients. At the inclusion we found no significant difference between patients with and without obesity for PaO₂/FiO₂ (204 [188–258] vs. 195 [178–300] mmHg), pH and PaCO₂ (Table S1). No patient suffered from hypercapnia above 50 mmHg.

All patients concluded the study and none had suffered from adverse events in both groups. Ventilatory settings in NAVA and in PSV are shown in Table S2. In PSV mode, PSV level exceeded 10 cmH₂O in 1 patient with obesity and 3 without obesity. In NAVA mode, NAVA level was never higher than 2 cmH₂O/µV. The monitored ventilatory variables and parameters are presented
<table><caption>**Table 1** Main characteristics of the 10 patients with obesity and the 11 patients without obesity included</caption><thead><tr><th>Patient</th><th>Obesity</th><th>Age (Yr)</th><th>Gender</th><th>Post-operative</th><th>Main diagnosis</th><th>Height (cm)</th><th>Weight (kg)</th><th>BMI (kg/m²)</th><th>SAPS II</th><th>Time between intubation and inclusion (days)</th><th>Inclusion and weaning (days)</th><th>Total duration of invasive ventilation (days)</th><th>Outcome</th></tr></thead><tbody><tr><td>With obesity</td><td>100%</td><td>65 [61–73]</td><td>20% F</td><td>70% Yes</td><td>-</td><td>171 [168–173]</td><td>100 [92–111]</td><td>35 [31–38]</td><td>60 [43–75]</td><td>3[2–5]</td><td>4[1–19]</td><td>10[3–23]</td><td>40% Died</td></tr><tr><td>1</td><td>Yes</td><td>63</td><td>M</td><td>Yes</td><td>Bowel obstruction</td><td>170</td><td>103</td><td>36</td><td>63</td><td>8</td><td>3</td><td>11</td><td>Survived</td></tr><tr><td>2</td><td>Yes</td><td>60</td><td>M</td><td>Yes</td><td>subdural empyema</td><td>173</td><td>91</td><td>31</td><td>57</td><td>3</td><td>11</td><td>14</td><td>Survived</td></tr><tr><td>3</td><td>Yes</td><td>66</td><td>M</td><td>Yes</td><td>hepatectomy</td><td>172</td><td>93</td><td>31</td><td>22</td><td>3</td><td>183</td><td>186</td><td>Died</td></tr><tr><td>4</td><td>Yes</td><td>48</td><td>M</td><td>Yes</td><td>Acute pancreatitis</td><td>172</td><td>113</td><td>38</td><td>39</td><td>2</td><td>0</td><td>2</td><td>Died</td></tr><tr><td>5</td><td>Yes</td><td>79</td><td>F</td><td>No</td><td>coma</td><td>155</td><td>76</td><td>32</td><td>77</td><td>1</td><td>1</td><td>2</td><td>Died</td></tr><tr><td>7</td><td>Yes</td><td>75</td><td>M</td><td>Yes</td><td>Peritonitis</td><td>176</td><td>124</td><td>40</td><td>70</td><td>1</td><td>1</td><td>2</td><td>Survived</td></tr><tr><td>9</td><td>Yes</td><td>68</td><td>M</td><td>Yes</td><td>acute cholecystitis</td><td>170</td><td>90</td><td>31</td><td>85</td><td>5</td><td>21</td><td>26</td><td>Died</td></tr><tr><td>16</td><td>Yes</td><td>35</td><td>M</td><td>No</td><td>Pneumonia</td><td>167</td><td>106</td><td>38</td><td>34</td><td>2</td><td>51</td><td>53</td><td>Survived</td></tr><tr><td>18</td><td>Yes</td><td>82</td><td>F</td><td>No</td><td>Stroke</td><td>157</td><td>97</td><td>39</td><td>76</td><td>8</td><td>1</td><td>9</td><td>Survived</td></tr><tr><td>20</td><td>Yes</td><td>62</td><td>M</td><td>Yes</td><td>Peritonitis</td><td>180</td><td>112</td><td>35</td><td>55</td><td>2</td><td>4</td><td>6</td><td>Survived</td></tr><tr><td>Without obesity</td><td>0%</td><td>69 [56–77]</td><td>45% F</td><td>45% Yes</td><td>-</td><td>165 [163–174]</td><td>68 [68–79]</td><td>26 [25–28]</td><td>48 [39–59]</td><td>2[1–6]</td><td>2[1–5]</td><td>4[3–9]</td><td>18% Died</td></tr><tr><td>6</td><td>No</td><td>51</td><td>F</td><td>Yes</td><td>Stroke</td><td>183</td><td>94</td><td>28</td><td>54</td><td>18</td><td>14</td><td>32</td><td>Survived</td></tr><tr><td>8</td><td>No</td><td>61</td><td>F</td><td>Yes</td><td>Acute pancreatitis</td><td>165</td><td>68</td><td>25</td><td>48</td><td>1</td><td>3</td><td>4</td><td>Survived</td></tr><tr><td>10</td><td>No</td><td>62</td><td>M</td><td>Yes</td><td>abdominal trauma</td><td>178</td><td>86</td><td>27</td><td>41</td><td>6</td><td>1</td><td>7</td><td>Survived</td></tr><tr><td>11</td><td>No</td><td>82</td><td>F</td><td>Yes</td><td>Subdural hematoma</td><td>160</td><td>67</td><td>26</td><td>42</td><td>3</td><td>0</td><td>3</td><td>Survived</td></tr><tr><td>12</td><td>No</td><td>78</td><td>F</td><td>No</td><td>Cardiac arrest</td><td>155</td><td>67</td><td>28</td><td>91</td><td>5</td><td>10</td><td>15</td><td>Died</td></tr><tr><td>13</td><td>No</td><td>79</td><td>M</td><td>No</td><td>Stroke</td><td>180</td><td>76</td><td>23</td><td>35</td><td>2</td><td>1</td><td>3</td><td>Died</td></tr><tr><td>14</td><td>No</td><td>69</td><td>M</td><td>No</td><td>Hepatic Coma</td><td>163</td><td>73</td><td>27</td><td>59</td><td>1</td><td>1</td><td>2</td><td>Survived</td></tr><tr><td>15</td><td>No</td><td>71</td><td>M</td><td>No</td><td>Pneumonia</td><td>170</td><td>82</td><td>28</td><td>60</td><td>2</td><td>2</td><td>4</td><td>Survived</td></tr><tr><td>17</td><td>No</td><td>50</td><td>M</td><td>No</td><td>Status epilepticus</td><td>163</td><td>68</td><td>26</td><td>37</td><td>1</td><td>2</td><td>3</td><td>Survived</td></tr><tr><td>19</td><td>No</td><td>76</td><td>F</td><td>No</td><td>Pneumonia</td><td>165</td><td>68</td><td>25</td><td>58</td><td>1</td><td>6</td><td>7</td><td>Survived</td></tr><tr><td>21</td><td>No</td><td>46</td><td>M</td><td>Yes</td><td>Liver injury</td><td>170</td><td>68</td><td>24</td><td>33</td><td>11</td><td>0</td><td>11</td><td>Survived</td></tr><tr><td>P</td><td>&lt;0.01</td><td>0.75</td><td>0.36</td><td>0.39</td><td></td><td>0.57</td><td>&lt;0.01</td><td>&lt;0.01</td><td>0.38</td><td>0.85</td><td>0.28</td><td>0.48</td><td>0.36</td></tr></tbody></table>

Summary data are presented as median [interquartile range]. P: P-value calculated between patients with and without obesity using Mann Whitney test. BMI: Body Mass Index; SAPS II: Simplified Acute Physiology Score II
in Table S3. Patients with obesity tend to have lower VT with NAVA versus PSV, respectively 6.7 mL/kg predicted body weight [5.9–7.1] versus 7.2 mL/kg [6.2–8.2], *p* < 0.05. In patients without obesity this difference was not significant. Minute ventilation was similar between NAVA and PSV. There was no significant difference in Max EADi between patients with or without obesity. In PSV mode it was 6.7 [4.1–11] µV in patient with obesity versus 8.8 [4.6–11.1] µV in patients without obesity (*p* = 0.38), and in NAVA mode it was 7 [4.5–10.4] versus 8.9 [4.9–9.5] (*p* = 0.627). Compared to PSV, NAVA was significantly associated with more respiratory cycles with Max P<sub>insp</sub> >30 cmH<sub>2</sub>O (Figure S3) and with VT < 5 ml/kg PBW (Table S4).

In patients with obesity, NAVA versus PSV was associated with a reduction in T<sub>d</sub> (0 [0–5] vs. 106 [34–125] ms, *p* < 0.05) and T<sub>iex</sub> (96 [94–102] vs. 145 [137–202] ms, *p* < 0.01). Patient-ventilator Dyssynchronies are reported in Table 2. A technical issue occurred in recording of respiratory cycles in 2 patients, thus 19 patients were analyzed for this part of the study. Despite the decrease in ineffective efforts (0 [0-0.03] vs. 0.33 [0.23-0.37] events/min, *p* < 0.05), the prevalence of total dyssynchronies was similar in NAVA and in PSV (2.2% [1.1-4.4] vs. 3.7% [2.4-5.6], *p* = 0.68). Indeed, the NAVA ventilation was associated with an increase in Type 1 double triggering. Figure 1 shows individual DI in NAVA and in PSV. DI exceeded 10% in patients without obesity in NAVA and in one patient with obesity in PSV. There was no significant difference between PSV and NAVA. Subgroup analysis by BMI showed no consistent trend or statistically significant differences between PSV and NAVA across BMI groups (Table S5).

Compared with baseline, the PaO₂/FiO₂ ratio was significantly higher at the end of NAVA ventilation but not at the end of PSV ventilation Fig. 2. No significant association was found between PaO₂/FiO₂ and variability of VT or Max P<sub>insp</sub> (Figure S4). Arterial pH, PaCO₂, PaO₂/FiO₂ were not significantly different between patients with and without obesity. Over the study period, Hemodynamics parameters, RASS and BPS scores were not significantly different between the two modes. The obesity factor was never significant.

Figure 3 represents the relationship between VT and Max P<sub>insp</sub> in NAVA and in PSV, in patients with and without obesity. Max P<sub>insp</sub> remained essentially constant in PSV mode across a range of VT, suggesting limited adaptation of support to the patient's effort. By contrast, in NAVA, Max P<sub>insp</sub> scaled with VT, showing more variability. Figures S5–S8 display individual patient-level pressure-volume relationships. Variability of all ventilatory parameters (RR, VT, Max P<sub>insp</sub>) are presented in Table S6. Ventilatory variability was significantly higher with NAVA, with a mean inspiratory airway pressure of 15

[10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21] % versus 3 [2, 3, 4] % in overall patients, 16% [11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21] versus 4% [2, 3, 4] in patients with obesity, 12 [9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20] % versus 3 [1, 2, 3] % in patients without obesity.

## Discussion

This study showed that NAVA ventilation was feasible and safe in critically ill patients with obesity, allowing a reduction in ineffective effort, an improvement in oxygenation and an increase of variability compared to PSV ventilation.

To our knowledge this is the first study to report the use of NAVA in the specific group of patients with obesity. The collection of the EADi signal has always been possible, and no patient was excluded in this group which confirms the feasibility and safety of NAVA in patients with obesity. Obesity does not appear to cause difficulty for the utilization of NAVA. In patients without obesity, only one was excluded because the EADi signal necessary for NAVA was absent. This lack of signal highlighted a diaphragmatic paralysis related to amyotrophic lateral sclerosis whose diagnosis was made posteriori. Diaphragmatic dysfunction is a known limitation of NAVA [25] as the neural stimulus of the diaphragm is used to trigger the ventilatory and to determine the level of pressure support provided.

NAVA ventilation was associated with a significant reduction in ineffective efforts in both groups of patients. Ineffective effort occurs when patient effort is insufficient to overcome the burden of intrinsic PEEP. While in PSV patients must overcome the intrinsic PEEP before triggering an inspiration, there is no possible influence of intrinsic PEEP in NAVA on the beginning of the cycle, since assistance begins with the patient's neural effort. Using a neural trigger allows to eliminate the link between hyperinflation and patient-ventilator dyssynchrony [3]. Moreover, in NAVA the inspiratory assistance is proportional to patient's effort which limiting the risk of over or under assistance, harmful to the diaphragm [26]. High pressure level leads to an increasing of tidal volume (which promotes intrinsic PEEP) and an inhibition of central control (which reduces the intensity of effort) which is at the origin of ineffective efforts [27].

Despite the reduction of ineffective effort with NAVA the dyssynchronies index was similar in NAVA and in PSV in contrast to previous reports [5, 12, 13, 28]. In these studies the authors found dysynchronies index between 12 and 40.2% in PSV and between 4, 5 to 10.8% in NAVA and the difference is always significantly in favor of NAVA. Compared to these studies, the incidence of patient ventilator dyssynchrony is very low in our work which may explain the absence of significant difference between NAVA and PSV. The lower incidence of patient
<table><caption>**Table 2** Total and specific dyssynchrony events for PSV and NAVA in all patients, with and without obesity</caption><thead><tr><th rowspan="2"></th><th colspan="3">All patients (n = 19)</th><th colspan="3">Patients with obesity (n = 9)</th><th colspan="3">Patients without obesity (n = 10)</th></tr><tr><th>PSV</th><th>NAVA</th><th>P</th><th>PSV</th><th>NAVA</th><th>P</th><th>PSV</th><th>NAVA</th><th>P</th></tr></thead><tbody><tr><td>T<sub>d</sub> (ms)</td><td>113 [34–152]</td><td>0 [0–10]</td><td>&lt;0.01</td><td>106 [34–125]</td><td>0 [0–5]</td><td>0.02</td><td>86 [9–156]</td><td>0 [0–12]</td><td>0.02</td></tr><tr><td>T<sub>ex</sub> (ms)</td><td>179 [124–218]</td><td>105 [97–110]</td><td>&lt;0.01</td><td>145 [137–202]</td><td>96 [94–102]</td><td>&lt;0.01</td><td>192 [133–249]</td><td>110 [107–117]</td><td>0.03</td></tr><tr><td>Total dyssynchronies (n/min)</td><td>0.6 [0.3–1.2]</td><td>0.6 [0.5–1.1]</td><td>0.71</td><td>0.9 [0.5–1.3]</td><td>0.6 [0.3–1]</td><td>1</td><td>0.5 [0.2–0.9]</td><td>0.6 [0.5–1.1]</td><td>0.63</td></tr><tr><td>DI (%)</td><td>3.1 [1.1–4.7]</td><td>2.2 [1.4–3.9]</td><td>0.77</td><td>3.7 [2.4–5.6]</td><td>2.2 [1.1–4.4]</td><td>0.68</td><td>1.7 [0.8–3.7]</td><td>2.6 [1.6–3.3]</td><td>0.37</td></tr><tr><td>Ineffective efforts (n/min)</td><td>0.27 [0.07–0.33]</td><td>0 [0–0]</td><td>&lt;0.01</td><td>0.33 [0.23–0.37]</td><td>0 [0–0.03]</td><td>0.02</td><td>0.17 [0.05–0.27]</td><td>0 [0–0]</td><td>0.02</td></tr><tr><td>Double triggering (n/min)</td><td>0.17 [0.03–0.38]</td><td>0.5 [0.33–1.02]</td><td>0.01</td><td>0.1 [0.03–0.43]</td><td>0.57 [0.23–1]</td><td>0.02</td><td>0.2 [0.06–0.33]</td><td>0.47 [0.35–0.93]</td><td>0.09</td></tr><tr><td>Double triggering type 1 (n/min)</td><td>0 [0–0]</td><td>0.37 [0.18–0.7]</td><td>&lt;0.01</td><td>0 [0–0]</td><td>0.4 [0.2–0.87]</td><td>&lt;0.01</td><td>0 [0–0]</td><td>0.33 [0.18–0.51]</td><td>&lt;0.01</td></tr><tr><td>Double triggering type 2 (n/min)</td><td>0.17 [0.03–0.38]</td><td>0.13 [0.05–0.2]</td><td>0.34</td><td>0.1 [0.03–0.43]</td><td>0.1 [0.03–0.2]</td><td>0.74</td><td>0.2 [0.06–0.33]</td><td>0.13 [0.07–0.19]</td><td>0.31</td></tr><tr><td>Auto triggering (n/min)</td><td>0.07 [0–0.13]</td><td>0 [0–0.07]</td><td>0.11</td><td>0.1 [0.07–0.17]</td><td>0.03 [0–0.1]</td><td>0.31</td><td>0.03 [0–0.11]</td><td>0 [0–0.03]</td><td>0.14</td></tr><tr><td>Premature cycling (n/min)</td><td>0.03 [0–0.07]</td><td>0 [0–0]</td><td>0.03</td><td>0.07 [0–0.13]</td><td>0 [0–0]</td><td>0.07</td><td>0.02 [0–0.06]</td><td>0 [0–0]</td><td>0.16</td></tr><tr><td>Late cycling (n/min)</td><td>0.03 [0–0.07]</td><td>0 [0–0.03]</td><td>0.12</td><td>0.03 [0–0.07]</td><td>0 [0–0.03]</td><td>0.40</td><td>0.02 [0–0.06]</td><td>0 [0–0]</td><td>0.20</td></tr></tbody></table>

Data are presented as median [interquartile range], P, Value calculated between PSV and NAVA using Wilcoxon test. PSV = Pressure Support Ventilation; NAVA = Neurally Adjusted Ventilatory Assist; DI = Dyssynchrony index n/min = Number of events/min; T<sub>d</sub> = inspiratory trigger delay; T<sub>ex</sub> = inspiratory time in excess

ventilator dyssynchronies in PSV in our study could have 3 explanations. The first is the absence of a patient with severe obstructive disease in our work in contrast to Schmidt et al., and Piquilloud et al. studies. Due to a higher intrinsic PEEP these patients are more likely to have a high incidence of dyssynchrony [29]. Second, we set the pressure support level lower than previous studies which limit the risk of over assistance. High level of assistance leads to an increasing of tidal volume (which promotes intrinsic PEEP) and an inhibition of central control (which reduces the intensity of effort) and causes patients ventilator dyssynchronies [27]. In this study, low level of pressure assistance probably could explain why incidence of patient-ventilator dyssynchronies are similar in NAVA and in PSV. Despite these low levels of pressure support, no patients suffer from respiratory clinical signs of self-inflicted lung injury (SILI) [30] and/or acidosis which confirms that our settings were adapted to the patients. Finally, Schmidt et al., Bertrand et al. and Piquilloud et al. studies compared NAVA and PSV in non-invasive ventilation and patient-ventilator dyssynchronies can be increased by leaks through the facemask [31].

As previously reported, there was more double triggering type 1 in NAVA [4, 5, 6, 13]. This increase is explained for technical reasons. As well described by Piquilloud et al. [5], the filtered Eadi signal used by NAVA to command the ventilator sometimes has a biphasic aspect. In NAVA, both triggering and cycling are driven by the EAdi. A fall in EAdi amplitude after the first peak is interpreted as end-inspiration, prompting cycling-off and termination of pressurization. A subsequent rise in EAdi (second peak) is then interpreted as the onset of a new inspiratory effort, leading the ventilator to deliver a second pressurization. This produces a NAVA-specific form of double triggering. Accordingly, we distinguish type 1 “technical” double triggering inherent to NAVA, and type 2 “standard” double triggering attributable to other causes. Type 1 double triggering is difficult to mitigate. Lowering trigger sensitivity may be deleterious with ineffective efforts and increased patient effort. Increasing the NAVA level can reduce effort and attenuate EAdi amplitude, thereby limiting the double peak. Type 2 double triggering management first seeks external contributors and then optimizes trigger sensitivity and the NAVA level.

In this study we found an improvement in oxygenation in NAVA compared to PSV. This improvement of oxygenation in NAVA is reported for long duration of NAVA [8] but not for short length. Several hypotheses could explain this improvement of oxygenation in NAVA. Mechanically ventilated patients with obesity have an increased risk of atelectasis and hypoxemia [17] and recruitment maneuver reduce the atelectasis and improved oxygenation [32]. The presence of more pneumatic cycles with Max P<sub>insp</sub> >30 cmH<sub>2</sub>O in NAVA could be assimilated to
<figure><img src="image_4.png" /><figcaption>**Fig. 1** Individual variation of the Dyssynchrony index (DI) for 19 of 21 patients, for 9 of 10 patients with obesity (Left) and for 10 of 11 patients without obesity (right) during Pressure Support Ventilation (PSV) and Neurally Adjusted Ventilatory Assist (NAVA). The horizontal bars represent the mean values</figcaption></figure>

alveolar auto-recruitment and could explain a better oxygenation. Moreover, compared to PSV there was no more breathing cycle with an excessive VT and NAVA should not increase the risk of ventilation induced injury. Better oxygenation could also be explained by an increasing of respiratory variability [33, 34] and the diminution of ineffective triggering in NAVA.

Obesity is characterized by reduced functional residual capacity, decreased chest-wall compliance, higher pleural/abdominal pressures, and greater atelectasis susceptibility, often necessitating higher PEEP and inspiratory pressures [17]. In this context, NAVA's effort-proportional assistance helps adapt pressurization to patient demand reducing lung collapse. NAVA also improves patient-ventilator synchrony, preserves physiologic variability, and limits both over- and under-assistance, which are associated with lung and diaphragm injury [26]. NAVA in patients with obesity was also associated with lower VT and higher respiratory rates than PSV with similar MV. Physiological studies found that, at baseline, obese subjects have higher RR and lower VT compared to non-obese subjects [35]. During an increase in

ventilatory demand (for example during an effort), these patients preferentially increase their respiratory rate and decrease their tidal volume [22]. Thus, the modification of breathing pattern in NAVA could correspond to a more physiological ventilation in patients with obesity. Difference in maximal EAdi between patients with and without obesity was not statistically significant. Although it could be thought that the EAdi signal intensity reflects a greater esophagus-diaphragm distance (as hypothesized in patients with obesity), it is in fact mainly influenced by the strength of the patient's inspiratory effort.

In overall patients we showed a Max P<sub>insp</sub> remained essentially constant in PSV mode across a range of VT, suggesting limited adaptation of support to the patient's effort. Achieving higher ventilation therefore required greater patient effort. By contrast, in NAVA, Max P<sub>insp</sub> scaled with VT, showing physiologically appropriate variability and indicating better coupling between neural drive and delivered pressure. Previous studies suggest the clinical benefit of increased breathing variability which was associated with successful ventilatory weaning [36,
<figure><img src="image_5.png" /><figcaption>**Fig. 2** Individual variations in PaO₂/FiO₂ ratio for 18 of 21 patients (**top**), for 9 of 10 patients with obesity (**middle**) and for 9 of 11 patients without obesity (**bottom**) after mechanical ventilation with Pressure Support Ventilation (**PSV**, **left**) and with Neurally Adjusted Ventilatory Assist (**NAVA**, **right**). The horizontal bars represent the mean values. PaO₂ = partial pressure of arterial oxygen; FiO₂ = inspired oxygen fraction; H 0 = baseline; H 30 = after 30 min of mechanical ventilation; \* *P* < 0.05 between H 0 and H 30</figcaption></figure>

[37], lower duration of mechanical ventilation [38] and higher survival rate [38, 39].

There are several limitations to this work. First, although the crossover design strengthens the validity of the results, the relatively small sample size limits the generalizability of the study. Second, the duration of

ventilation in our study was probably too short to evaluate the long term safety of NAVA ventilation patients with obesity. As it is a physiological study, the effect of the NAVA on morbidity and prognosis for patients with obesity has not been studied. Third, our group of patients with obesity was mostly comprised of moderate to severe
<figure><img src="image_6.png" /><figcaption>**Fig. 3** Scatter plots of Maximal inspiratory airway pressure (Max P<sub>insp</sub>, cmH2O) vs. tidal volume (VT, mL/kg) measured in all patients (top), with obesity (middle) and without obesity (bottom) during Pressure Support Ventilation (PSV, left) and Neurally Adjusted Ventilatory Assist (NAVA, right). Lines represent linear regression lines</figcaption></figure>

obesity (BMI = 35 kg/m² median). Further studies are necessary to evaluate NAVA in a population of morbidly obese (BMI > 40 kg/m²). Similarly, patients without obesity were nonetheless overweight, with a median BMI of 26 kg/m². This reflects consecutive enrollment, participants were not selected on the basis of BMI. Fourth, the higher incidence of ineffective efforts during PSV may be attributed to an excessively high flow trigger [27]. However, the trigger sensitivity was set to a very low (i.e., highly sensitive) value, which could conversely increase the risk of self-triggering.

Further studies in larger cohorts including morbidly obese patients, with longer follow-up, are needed to confirm the clinical benefits of NAVA (improved trigger precision, enhanced ventilatory variability, and better oxygenation) on outcomes such as weaning success, ventilation duration and mortality in patients with obesity.

## Conclusion

This study reports for the first time the feasibility and the safety of NAVA in patients with obesity. The NAVA has reduced the ineffective efforts and improved oxygenation in patients with obesity compared to PSV. Subsequent
studies on the interest of NAVA on the duration of wean-
ing and respiratory prognosis of patients with obesity
could be considered.

Abbreviations

<table>
   <tr>
    <td>
     BMI
    </td>
    <td>
     Body Mass Index
    </td>
   </tr>
   <tr>
    <td>
     BPS
    </td>
    <td>
     Behavioral Pain Scale
    </td>
   </tr>
   <tr>
    <td>
     DI
    </td>
    <td>
     Dyyssynchrony Index
    </td>
   </tr>
   <tr>
    <td>
     EADI
    </td>
    <td>
     Electrical Activity of the Diaphragm
    </td>
   </tr>
   <tr>
    <td>
     EMG
    </td>
    <td>
     Electromyogram
    </td>
   </tr>
   <tr>
    <td>
     FiO2
    </td>
    <td>
     Inspired Oxygen Fraction
    </td>
   </tr>
   <tr>
    <td>
     ICU
    </td>
    <td>
     Intensive Care Unit
    </td>
   </tr>
   <tr>
    <td>
     MV
    </td>
    <td>
     Minute Ventilation
    </td>
   </tr>
   <tr>
    <td>
     NAVA
    </td>
    <td>
     Neurally Adjusted Ventilatory Assist
    </td>
   </tr>
   <tr>
    <td>
     PaCO2
    </td>
    <td>
     Arterial Partial Pressure of Carbon Dioxide
    </td>
   </tr>
   <tr>
    <td>
     PaO2
    </td>
    <td>
     Arterial Partial Pressure of Oxygen
    </td>
   </tr>
   <tr>
    <td>
     PBW
    </td>
    <td>
     Predicted Body Weight
    </td>
   </tr>
   <tr>
    <td>
     PEEP
    </td>
    <td>
     Positive End Expiratory Pressure
    </td>
   </tr>
   <tr>
    <td>
     Pins
    </td>
    <td>
     Inspiratory Pressure
    </td>
   </tr>
   <tr>
    <td>
     PSV
    </td>
    <td>
     Pressure Support Ventilation
    </td>
   </tr>
   <tr>
    <td>
     RASS
    </td>
    <td>
     Richmond Agitation Sedation Scale
    </td>
   </tr>
   <tr>
    <td>
     RR
    </td>
    <td>
     Respiratory Rate
    </td>
   </tr>
   <tr>
    <td>
     SAPS II
    </td>
    <td>
     Simplified Acute Physiology Score II
    </td>
   </tr>
   <tr>
    <td>
     Td
    </td>
    <td>
     Trigger delay
    </td>
   </tr>
   <tr>
    <td>
     Ti
    </td>
    <td>
     Inspiratory Time
    </td>
   </tr>
   <tr>
    <td>
     Tiex
    </td>
    <td>
     Time in excess
    </td>
   </tr>
   <tr>
    <td>
     Ttot
    </td>
    <td>
     Totale Respiratory Time
    </td>
   </tr>
   <tr>
    <td>
     VT
    </td>
    <td>
     Tidal Volume
    </td>
   </tr>
  </table>

**Supplementary Information**

The online version contains supplementary material available at https://doi.org/10.1186/s13613-025-01552-x.

Supplementary Material 1

Acknowledgements

Not applicable.

Author contributions

MCo, SJ, ADJ and MCa drafted the manuscript. MCo and SJ designed the study. NM and ADJ wrote the statistical analysis plan, estimated the sample size and are involved in data analysis. MCo and FG are involved in the intervention and data acquisition. All authors MCo SJ FG NM GC ADJ MCa revised the manuscript for important intellectual content and read and approved the final version of the manuscript.

Funding

Not applicable.

Data availability

The datasets used and/or analysed during the current study are available from
the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

The institutional review board (Comité de Protection des Personnes Sud Méditéérannée IV, Montpellier, France) approved the protocol (ref number: 2009-A00087-50). Written informed consent was provided by the patient or surrogates.

Consent for publication

Not applicable.

Competing interests

SJ reports receiving consulting fees from Drager, Mindray, Medtronic, Baxter, Fresenius-Xenios and Fisher & Paykel. ADJ reports receiving consulting fees

from Viatris, Medtronic, and Sanofi. No potential conflict of interest relevant to
this article was reported for other authors.

Author details

¹Department of Anaesthesiology and Critical Care Medicine B (DAR B), Saint-Eloi Hospital, University Teaching Hospital of Montpellier, 80 avenue Augustin Fliche, Montpellier 34295, France

²INSERM U1046 PhyMedExp, Montpellier, France

³Department of Statistics, University of Montpellier Lapeyronie Hospital, UMR 729 MISTEA, 371 Av. du Doyen Gaston Giraud, Montpellier 34090, France

Received: 23 April 2025 / Accepted: 21 August 2025

Published online: 29 August 2025

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