0
Original Research: CRITICAL CARE MEDICINE |

Inspiratory Muscle Unloading by Neurally Adjusted Ventilatory Assist During Maximal Inspiratory Efforts in Healthy Subjects* FREE TO VIEW

Christer Sinderby, PhD; Jennifer Beck, PhD; Jadranka Spahija, PhD; Michel de Marchie, MD; Jacques Lacroix, MD; Paolo Navalesi, MD; Arthur S. Slutsky, MD
Author and Funding Information

*From the Department of Critical Care Medicine (Drs. Sinderby and Slutsky), St. Michael’s Hospital, Department of Medicine, University of Toronto, Toronto, ON, Canada; Department of Newborn and Developmental Pediatrics (Dr. Beck), Sunnybrook Health Sciences Centre, Department of Pediatrics, University of Toronto, Toronto, ON, Canada; Sacré-Coeur Hospital Research Center (Dr. Spahija), Department of Medicine, University of Montreal, Montreal, QC, Canada; Sir Mortimer B. Davis Jewish General Hospital (Dr. Marchie), McGill University, Montreal, QC, Canada; Pediatric Intensive Care Unit, Department of Pediatrics (Dr. Lacroix), Hôpital Sainte-Justine Research Center, Université de Montréal, Montreal, QC, Canada; and Pulmonary Rehabilitation and Respiratory Intensive Care Unit (Dr. Navalesi), Fondazione S. Maugeri, Pavia, Italy.

Correspondence to: Christer Sinderby, PhD, Department of Critical Care, St. Michael’s Hospital, University of Toronto, 30 Bond Street, Queen 4–072, Toronto, ON, Canada, M5B 1W8; e-mail: sinderby@rogers.com



Chest. 2007;131(3):711-717. doi:10.1378/chest.06-1909
Text Size: A A A
Published online

Background: Neurally adjusted ventilatory assist (NAVA) is a mode of mechanical ventilation in which the ventilator is controlled by the electrical activity of the diaphragm (EAdi). During maximal inspirations, the pressure delivered can theoretically reach extreme levels that may cause harm to the lungs. The aims of this study were to evaluate whether NAVA could efficiently unload the respiratory muscles during maximal inspiratory efforts, and if a high level of NAVA would suppress EAdi without increasing lung-distending pressures.

Method: In awake healthy subjects (n = 9), NAVA was applied at increasing levels in a stepwise fashion during quiet breathing and maximal inspirations. EAdi and airway pressure (Paw), esophageal pressure (Pes), and gastric pressure, flow, and volume were measured.

Results: During maximal inspirations with a high NAVA level, peak Paw was 37.1 ± 11.0 cm H2O (mean ± SD). This reduced Pes deflections from − 14.2 ± 2.7 to 2.3 ± 2.3 cm H2O (p < 0.001) and EAdi to 43 ± 7% (p < 0.001), compared to maximal inspirations with no assist. At high NAVA levels, inspiratory capacity showed a modest increase of 11 ± 11% (p = 0.024).

Conclusion: In healthy subjects, NAVA can safely and efficiently unload the respiratory muscles during maximal inspiratory maneuvers, without failing to cycle-off ventilatory assist and without causing excessive lung distention. Despite maximal unloading of the diaphragm at high levels of NAVA, EAdi is still present and able to control the ventilator.

Figures in this Article

Neurally adjusted ventilatory assist (NAVA) is a mode of mechanical ventilation in which positive pressure is applied to the airway opening in proportion to the electrical activation of the diaphragm (EAdi).1 With NAVA, ventilator support is initiated when the neural drive to the diaphragm begins to increase. As the EAdi progressively increases, the assist increases proportionally and, most importantly, the pressure delivered by the ventilator is cycled-off when the EAdi is ended by the respiratory centers. The amount of assist delivered during NAVA depends on a proportionality factor, the so-called “NAVA level,” which defines the magnitude of pressure delivered for a given EAdi. When the NAVA level is changed, the resulting pressure delivered by the ventilator depends on how the respiratory afferents modulate the neural output to the diaphragm. If the response to an increase in NAVA is not a reduction in the EAdi, the delivered pressure increases. However, a reflexive or involuntary reduction in EAdi would mitigate the effects of an increased NAVA level, and the delivered pressure may remain unchanged or be less than anticipated.

Thus, the response in EAdi to an increase in the NAVA level determines the resulting transpulmonary pressure (Ptp) and whether volume changes or not. Consequently, during maximal inspirations, when the EAdi is at its highest,2the pressure delivered could reach extreme levels that may cause harm to the lungs.3 It is therefore important to determine with increasing NAVA levels whether or not the EAdi is suppressed thereby limiting the pressure delivered during maximal inspiration. Based on the above, the aims of the present study were to determine the following: (1) whether NAVA efficiently unloads respiratory muscles throughout a maximal inspiration in healthy subjects, and (2) if EAdi is suppressed during maximal inspirations with increasing levels of NAVA.

Subjects

Nine healthy subjects (one woman) were studied. Their mean (± SD) age, height, and weight were 37 ± 8 years, 172 ± 7 cm, and 71 ± 8 kg, respectively. Two subjects had prior knowledge of mechanical ventilation. The study was approved by the Scientific and Ethical Committees of Sainte-Justine’s Hospital, Montreal, Canada, and all subjects gave their informed consent.

Measurements

Electrical signals of the diaphragm were obtained using a multiple-array esophageal electrode (nine electrodes spaced 10-mm apart). Balloons were mounted on the same catheter for measurements of esophageal pressure (Pes), gastric pressure (Pga), and transdiaphragmatic pressure (Pdi). Flow was measured with a pneumotachograph (No. 2; Hewlett Packard; Palo Alto, CA) connected to a pressure transducer (± 3 cm H2O; Ohmega Engineering; Stanford, CT). Airway pressure (Paw) was measured with a pressure sensor (± 350 cm H2O; Sensym; Milpitas, CA) and was placed with the pneumotach between the mouthpiece and the ventilator (Servo 300; Maquet Critical Care; Solna, Sweden). Respiratory inductance plethysmography (Respitrace; Ambulatory Monitoring; Ardsley, NY) was used to evaluate rib cage and abdominal displacements. All signals were acquired simultaneously, displayed on-line to the investigators, and stored for off-line analysis.

EAdi Signal Processing

Signal processing of EAdi followed American Thoracic Society recommendations.4Filters and algorithms giving the highest possible signal-to-disturbance ratio were applied.5 Changes in diaphragm position along the array were accounted for,56 yielding a signal not artifactually affected by changes in lung volume or chest wall configuration.78 The root-mean-square was used to quantify EAdi every 16 ms.910 Signal segments with residual disturbances were replaced by the previously accepted value, resulting in a processed EAdi signal.

Method for NAVA

The processed EAdi was used to control a Servo 300 ventilator according to Sinderby et al.1 NAVA is based on transforming the EAdi amplitude into a voltage every 16 ms and sending it to the Servo 300 ventilator, which responds by adjusting the pressure level according to a linear function. The EAdi can be multiplied by a number, which essentially is a proportionality factor determining the amount of pressure is delivered for a given EAdi. This factor is referred to as the NAVA level in the present work, but has also been referred to as NAVA gain in a previous publication.,1 With an increase in the NAVA level, more pressure is delivered by the ventilator if the EAdi (ie, respiratory drive) does not decrease.

In the current application, NAVA was applied during inspiration, and the assist was cycled-off to zero positive end-expiratory pressure. For triggering on, ventilatory assist was initiated when the EAdi exceeded a threshold increment in EAdi. Given that the variability of the noise level was low, the trigger threshold was set to a fixed level that permitted early detection of increasing diaphragm activation without causing autotriggering when the diaphragm was inactive. For cycling-off, ventilatory assist was terminated when the EAdi fell below a percentage (default 80%) of peak inspiratory activity.

Experimental Protocol

Subjects were studied in sitting position, breathing at rest through a mouth piece connected to the ventilator. Subjects breathed at rest for 3 to 5 min and performed at least two maximal inspirations toward the end of the period. This was subsequently repeated with increasing NAVA levels, as long as increasing NAVA levels decreased the negative Pes deflection observed on the computer monitor. In the present study, no positive end-expiratory pressure was applied.

Analysis

The start and end of each maximal inspiration were determined using the flow signal. For each tidal or maximal inspiration, EAdi signal strength was calculated as the mean inspiratory EAdi with a baseline EAdi subtracted (mean electrical activity of the diaphragm [XEAdi]). The mean pressure swings for Paw (mean Paw [XPaw]), Pes (mean Pes [XPes]), Pga (mean Pga [XPga]), Pdi, and Ptp (mean Ptp [XPtp]) were also calculated. Volume was obtained by integration of the flow signal.

In order to compare the same conditions for the different subjects, the runs were classified into three NAVA levels. Zero NAVA level refers to the condition in which the subject was breathing on the ventilator circuit without assist. High NAVA was the highest level applied (abolishing or reversing the swing in Pes), and intermediate NAVA was the NAVA level when XPaw was approximately 50% of that observed during the highest NAVA level.

Statistical Analysis

Repeated-measures analysis of variance was used to compare variables between different levels of NAVA. Post hoc comparison was performed with a Tukey test. Correlation between the mean and peak pressures was performed with Pearson product moment correlation. The statistical analyses were performed using statistical software (Sigmastat, version 2.0; Jandel Scientific; San Rafael, CA). The level of significance for all statistical tests was p < 0.05. Data are presented as mean ± SD.

During both breathing at rest and maximal inspirations, NAVA was well tolerated by the subjects at all NAVA levels. In all subjects, it was possible to increase the NAVA to a level where the negative Pes deflection generated during the inspiratory capacity (IC) maneuver was abolished or reversed to positive. The group mean data obtained during the quiet breathing periods (zero and high NAVA level) are shown in Table 1 .

Figure 1 shows representative tracings for one subject performing maximal inspirations at zero, intermediate, and high levels of NAVA. The tracings show that increasing NAVA levels increased Paw and reduced Pes and Pdi. At the intermediate NAVA level (Fig 1), the negative deflection in Pes was reduced; with high NAVA levels, the Pes deflection was reversed from negative to positive, such that the deflection in Pdi was abolished. Despite the abolished Pdi deflection, the peak EAdi at high NAVA was reduced to only 40% of the value observed during the maximal inspiration with zero NAVA. Maximal inspiratory volumes increased only slightly with increasing NAVA levels.

For the group, data from the maximal inspirations reveal that both XPaw and XPes increased significantly from zero NAVA to intermediate NAVA (p = 0.001 and p < 0.001) and from intermediate to high NAVA levels (p < 0.001 and p < 0.001), respectively (Fig 2 ). Note that the increases in XPaw and XPes were parallel such that their difference, the XPtp, was not altered with increasing NAVA. The data are also presented for the resting breathing period (zero and high NAVA level). No significant changes were observed between zero, intermediate, and high NAVA levels for XPga (4.7 ± 5.2 cm H2O, 4.9 ± 3.9 cm H2O, and 6.5 ± 3.5 cm H2O, respectively) during the maximal inspirations. The correlation between the peak and mean values of Paw was r = 0.96 ± 0.03, and for the peak and mean values of Pes was r = 0.97 ± 0.01.

The peak Paw values during maximal inspirations at intermediate and high NAVA levels were 26.6 ± 8.7 cm H2O and 37.1 ± 11.0 cm H2O, respectively. Increasing NAVA from zero to intermediate reduced XEAdi during the maximal inspirations to 64 ± 14% (p < 0.001). The intermediate NAVA level was 40 ± 8% of that applied during high NAVA. A further increase from intermediate to high NAVA levels reduced EAdi to 43 ± 7% (p < 0.001) of baseline (Fig 3 ). IC did not change significantly between zero and intermediate NAVA, whereas it increased by 11 ± 11% (p = 0.024) from zero NAVA to high NAVA (Fig 3). In absolute values, IC was 2.77 ± 0.73 L, 2.92 ± 0.76 L, and 3.06 ± 0.86 L during zero, intermediate, and high NAVA levels, respectively.

At high levels of NAVA, EAdi was never suppressed completely. Figure 4 shows that EAdi was clearly present during both quiet breathing and maximal inspirations even when a high NAVA level eliminated deflections in Pdi. Despite the elimination of inspiratory Pdi, the remaining EAdi allowed subjects to control ventilator pressure delivery both in terms of timing and magnitude, independent of inspired volume. Analysis of chest wall configuration did not reveal any systematic changes between maximal inspirations with zero and high NAVA levels.

The present study demonstrates that NAVA can unload the respiratory muscles of a healthy subject to a level at which it substitutes the inspiratory muscle contribution to distend the lungs at all lung volumes. At such a high NAVA level, the subject still maintains the breathing pattern and full voluntary control of the ventilatory assist. This study also demonstrates that maximal inspirations performed with a high level of NAVA suppress the diaphragm electrical activity, thereby limiting increases in lung-distending pressures and volumes. No problems to cycle-off the assist were observed with increasing NAVA levels.

Unloading With NAVA

Since NAVA is controlled by the EAdi, the subject can control the delivered pressure when NAVA is increased by adjusting the neural output from the respiratory centers. Therefore, a subject should be able to either do the following: (1) keep the same EAdi, allowing the increased NAVA level to directly translate into increased Paw; or (2) maintain Paw unchanged by counteracting the increased NAVA level by reducing the EAdi. In the present study, the subjects demonstrated an intermediate response, where increasing the NAVA level both increased Paw and reduced EAdi, which in turn resulted in decreased Pes and decreased Pdi. This agrees well with a previous study11 suggesting that respiratory assist relieves the inspiratory muscle workload, allowing respiratory drive to be reduced.

An interesting finding of the present study was that the changes in XPaw and XPes were equal, keeping the XPtp unchanged (Fig 2). In other words, with each increased level of NAVA, the ventilator pressure delivery increased to substitute the inspiratory pressure generated by the subject without altering the XPtp during tidal and maximal inspirations. The same relationship (maintained XPtp with increasing NAVA levels) has previously demonstrated in tracheotomized, anesthetized, and spontaneously breathing animals with acute lung injury.12 This strongly supports a close interaction between NAVA, the neural respiratory feedback mechanisms, and the EAdi output.

Another interesting finding was that the EAdi, although suppressed, ensured control of ventilatory assist during both quiet breathing and maximal inspirations, even at the highest NAVA levels. In some subjects (Fig 1, 4), high NAVA resulted in a positive Pes deflection large enough to eliminate Pdi, suggesting that the diaphragm was nearly 100% unloaded, while EAdi was still clearly present. In 1962, Agostoni13 showed that increasing “positive pressure breathing” produced a progressive reduction in Pdi despite small changes in diaphragm electrical activity, and that pressures of approximately 30 cm H2O could eliminate Pdi during quiet breathing while diaphragm electrical activity remained.

Termination of Maximal Inspiration

Despite 55 years having passed since Mills14published the first article describing what limits the effort and depth of a voluntary maximal inspiration in a human, there is no consensus on this topic. Although this topic may be of academic relevance only in situations when maximal inspirations are performed without a ventilator, the introduction of a new generation of ventilators that deliver assist in proportion to the patient’s effort revives the question of whether diaphragm activity is downregulated with increasing levels of assist to prevent excessive lung-distending pressures during a maximal inspiration. More importantly, considering the current findings that lower tidal volumes may reduce ventilator-induced lung injury,15 knowledge about the possible presence/activity of lung-protective reflexes during neurally controlled mechanical ventilation is important.

Mills14 demonstrated an antagonistic abdominal muscle activation observed at the end of maximal inspiration that was accompanied by a closing of the glottis. Campbell and Green16showed that voluntary and unassisted maximal inspirations are terminated in association with increased electrical activation of abdominal muscles and a sharp rise in abdominal pressure. Both studies suggest that reflex inhibition terminates maximal inspirations in healthy subjects. Later, Agostoni and Rahn17demonstrated that active antagonistic abdominal muscle activation at maximal inspiration counterbalances the diaphragm activity and limits further expansion of the lung, which could protect the lung without involving reflexes. Mead et al18 demonstrated that with practice, both antagonistic abdominal muscle activation and closing of the glottis could be avoided at the end of maximal inspiration, and suggested that the maximum volume is determined by a balance arising from the elastic recoil of the respiratory system and the diminishing effectiveness of the inspiratory muscles at high lung volumes. In support of this finding, our group has previously demonstrated that the maximal voluntary activation of the diaphragm was similar during combined maximal inspiratory efforts against occluded airways at functional residual capacity and at total lung capacity in healthy subjects and in patients with diaphragm weakness,2 and that the pressure-generating capacity at total lung capacity decreases to approximately 40 cm H2O,,8 which is comparable to the Paw required to inflate the lungs in the present study.

Regardless of the mechanism, the present study shows that application of a high NAVA level during maximal inspiration strongly suppresses XEAdi, limiting the XPtp, and increases IC modestly in healthy subjects. These findings along with our previous work12 in tracheotomized lung-injured rabbits support the possible role of lung-protective reflexes during neurally controlled mechanical ventilation. However, it should be noted that healthy subjects were evaluated in the present study, and therefore the reflex effects may be different from those of patients with respiratory failure.

Critique of the Study

The present study could be criticized for several reasons. First, the present study was performed in healthy, awake subjects, which today is not conventional for studies on control of breathing. However, awake subjects were a requirement since the main intervention was maximal voluntary inspirations.

Second, while breathing at rest, the tidal volume and minute ventilation were greater than anticipated. This was likely due to the increased dead space of the tubing, connectors, pneumotachograph, and the mouthpiece. However, since tidal volume and minute ventilation did not change between zero and high NAVA levels while breathing at rest, we do not expect that this offset of the respiratory drive would effect mechanical unloading with NAVA.

Third, for safety reasons, we used a nonsealing mouthpiece. Thus, we cannot exclude that the slight but significant increase in IC at high NAVA levels may have been caused by leaks around the mouthpiece or nose clip.

NAVA can efficiently unload the respiratory muscles at all lung volumes. Diaphragm electrical activity is downregulated with increasing NAVA level, limiting lung distension during maximal inspirations in healthy subjects. The findings of the present study suggest that NAVA is well integrated with respiratory control systems and provides assist in response to central respiratory output. Despite maximal unloading of the diaphragm at high levels of NAVA, EAdi is still present and able to control the ventilator.

Abbreviations: EAdi = electrical activity of the diaphragm; IC = inspiratory capacity; NAVA = neurally adjusted ventilatory assist; Paw = airway pressure; Pdi = transdiaphragmatic pressure; Pes = esophageal pressure; Pga = gastric pressure; Ptp = transpulmonary pressure; XEAdi = mean electrical activity of the diaphragm; XPaw = mean airway pressure; XPes = mean esophageal pressure; XPga = mean gastric pressure; XPtp = mean transpulmonary pressure

The work was performed at Hôpital Sainte-Justine in Montreal, Quebec, Canada.

This work was supported in part by the Canadian Intensive Care Foundation. Dr. Beck and Dr. Sinderby were supported by the Fonds de la Recherche en Santé du Québec.

This disclosure statement has been approved by St-Michael’s Hospital, Sunnybrook Health Sciences Centre, and University of Toronto. Dr. Beck and Dr. Sinderby have made inventions related to neural control of mechanical ventilation that are patented. The license for these patents belongs to Maquet Critical Care. Future commercial uses of this technology may provide financial benefit to Dr. Sinderby and Dr. Beck through royalties. Dr. Sinderby and Dr. Beck each own 50% of Neurovent Research Inc. Neurovent Research is a research and development company that builds the equipment and catheters for research studies. Neurovent Research has a consulting agreement with Maquet Critical Care. Dr. Slutsky consults for companies that make ventilators, specifically Maquet Critical Care and Hamilton Medical and is compensated for these consultations. Drs. Spahija, de Marchie, Lacroix, and Navalesi have no conflicts of interest to disclose.

Table Graphic Jump Location
Table 1. Group Mean Values for Ventilatory Parameters, Timing Parameters, and Inspiratory Diaphragm Activity and Pressure Swings Obtained During Quiet Breathing With Zero NAVA and During High NAVA Level*
* 

Data are presented as mean ± SD; au = arbitrary units; XPdi = mean Pdi; NS = not significant.

Figure Jump LinkFigure 1. Time tracings of EAdi, volume, Paw, Pes, and Pdi during maximal inspirations with zero, intermediate, and high NAVA levels in an individual representative subject. Increasing NAVA increased deflections in Paw and reduced EAdi by approximately 60%. The negative inspiratory deflection in Pes was reduced with intermediate NAVA and reversed to a positive deflection with high NAVA. Pdi deflections were eliminated with high NAVA level.Grahic Jump Location
Figure Jump LinkFigure 2. Group mean values (± SD) for XPaw and XPes during maximal inspirations (open symbols) with zero, intermediate, and high NAVA levels and during quiet breathing (solid symbols) with zero and high NAVA levels. Dashed diagonal lines identify combinations of Pes and Paw representing similar lung-distending pressures (iso-Ptp lines). Note that the iso-Ptp lines represent a mean value. During maximal inspirations, the increase in NAVA from zero to intermediate increased XPaw (p < 0.001) and XPes (p < 0.001). Increases from intermediate to high NAVA further increased XPaw (p < 0.001) and changed XPes from negative values to positive (p < 0.001). During quiet breathing, increasing NAVA from zero to high increased XPaw (p < 0.001) and XPes (p < 0.001). All changes in XPaw and XPes observed during changes in NAVA followed the iso-Ptp lines.Grahic Jump Location
Figure Jump LinkFigure 3. Percentage changes in IC and XEAdi during maximal inspirations with zero, intermediate, and high NAVA levels. Increasing the NAVA produced a large decrease in XEAdi with a relatively small increase in IC. Values are presented as mean ± SD. *Denotes significant difference (p < 0.05) from zero NAVA. !Denotes significant difference (p < 0.05) from intermediate NAVA level.Grahic Jump Location
Figure Jump LinkFigure 4. Time tracing of volume, EAdi, Paw, Pes, Pga, and Pdi during two resting breaths (quiet breathing [QB]) and one maximal inspiration with high NAVA in one typical subject. Deflections in Pes and Pga are almost identical rendering an almost flat Pdi regardless of inspiratory volume achieved. The EAdi is clearly present and can adequately control proportional delivery of assist (Paw) during both resting and maximal inspirations.Grahic Jump Location
Sinderby, C, Navalesi, P, Beck, J, et al (1999) Neural control of mechanical ventilation.Nat Med5,1433-1436. [PubMed] [CrossRef]
 
Sinderby, C, Beck, J, Weinberg, J, et al Voluntary activation of the human diaphragm in health and disease.J Appl Physiol1998;85,2146-2158. [PubMed]
 
Tremblay, LN, Slutsky, AS Ventilator induced lung injury: from barotrauma to biotrauma.Proc Assoc Am Phys1998;110,482-488. [PubMed]
 
Aldrich, T, Sinderby, C, McKenzie, D, et al Electrophysiologic techniques for the assessment of respiratory muscle function. ATS/ERS statement on respiratory muscle testing.Am J Respir Crit Care Med2002;166,518-624. [PubMed]
 
Sinderby, C, Beck, JC, Lindström, L, et al Enhancement of signal quality in esophageal recordings of diaphragm EMG.J Appl Physiol1997;82,1370-1377. [PubMed]
 
Beck, J, Sinderby, C, Lindström, L, et al Influence of bipolar electrode positioning on measurements of human crural diaphragm EMG.J Appl Physiol1996;81,1434-1449. [PubMed]
 
Beck, J, Sinderby, C, Lindstrom, L, et al Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration.J Appl Physiol1997;82,520-530. [PubMed]
 
Beck, J, Sinderby, C, Lindstrom, L, et al Effects of lung volume on diaphragm EMG signal strength during voluntary contractions.J Appl Physiol1998;85,1123-1134. [PubMed]
 
Sinderby, C, Spahija, J, Beck, J, et al Diaphragm activation during exercise in chronic obstructive pulmonary disease.Am J Respir Crit Care Med2001;163,1637-1641. [PubMed]
 
Sinderby, C, Spahija, J, Beck, J Changes in respiratory effort sensation over time and its link to diaphragm sarcolemma excitability.Am J Respir Crit Care Med2001;163,905-910. [PubMed]
 
Georgopoulos, D, Roussos, C Control of breathing in mechanically ventilated patients.Eur Respir J1996;9,2151-2160. [PubMed]
 
Allo JC, Beck J, Brander L, et al. Influence of neurally adjusted ventilatory assist (NAVA) and PEEP on breathing pattern in rabbits with acute lung injury. Crit Care Med 2006 (in press).
 
Agostoni, E Diaphragm activity and thoracoabdominal mechanics during positive pressure breathing.J Appl Physiol1962;17,215-220. [PubMed]
 
Mills, JN The nature of the limitation of maximal inspiratory and expiratory efforts.J Physiol (Lond)1950;111,376-381. [PubMed]
 
The Acute Respiratory Distress Syndrome Network.. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.N Engl J Med2000;342,1301-1308. [PubMed]
 
Campbell, EJ, Green, JH The variations in intra-abdominal pressure and the activity of the abdominal muscles during breathing; a study in man.J Physiol (Lond)1953;122,282-290. [PubMed]
 
Agostoni, E, Rahn, HJ Abdominal and thoracic pressures at different lung volumes.J Appl Physiol1960;15,1087-1092. [PubMed]
 
Mead, J, Milic-Emili, J, Turner, JM Factors limiting depth of a maximal inspiration in human subjects.J Appl Physiol1963;18,295-296. [PubMed]
 

Figures

Figure Jump LinkFigure 1. Time tracings of EAdi, volume, Paw, Pes, and Pdi during maximal inspirations with zero, intermediate, and high NAVA levels in an individual representative subject. Increasing NAVA increased deflections in Paw and reduced EAdi by approximately 60%. The negative inspiratory deflection in Pes was reduced with intermediate NAVA and reversed to a positive deflection with high NAVA. Pdi deflections were eliminated with high NAVA level.Grahic Jump Location
Figure Jump LinkFigure 2. Group mean values (± SD) for XPaw and XPes during maximal inspirations (open symbols) with zero, intermediate, and high NAVA levels and during quiet breathing (solid symbols) with zero and high NAVA levels. Dashed diagonal lines identify combinations of Pes and Paw representing similar lung-distending pressures (iso-Ptp lines). Note that the iso-Ptp lines represent a mean value. During maximal inspirations, the increase in NAVA from zero to intermediate increased XPaw (p < 0.001) and XPes (p < 0.001). Increases from intermediate to high NAVA further increased XPaw (p < 0.001) and changed XPes from negative values to positive (p < 0.001). During quiet breathing, increasing NAVA from zero to high increased XPaw (p < 0.001) and XPes (p < 0.001). All changes in XPaw and XPes observed during changes in NAVA followed the iso-Ptp lines.Grahic Jump Location
Figure Jump LinkFigure 3. Percentage changes in IC and XEAdi during maximal inspirations with zero, intermediate, and high NAVA levels. Increasing the NAVA produced a large decrease in XEAdi with a relatively small increase in IC. Values are presented as mean ± SD. *Denotes significant difference (p < 0.05) from zero NAVA. !Denotes significant difference (p < 0.05) from intermediate NAVA level.Grahic Jump Location
Figure Jump LinkFigure 4. Time tracing of volume, EAdi, Paw, Pes, Pga, and Pdi during two resting breaths (quiet breathing [QB]) and one maximal inspiration with high NAVA in one typical subject. Deflections in Pes and Pga are almost identical rendering an almost flat Pdi regardless of inspiratory volume achieved. The EAdi is clearly present and can adequately control proportional delivery of assist (Paw) during both resting and maximal inspirations.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Group Mean Values for Ventilatory Parameters, Timing Parameters, and Inspiratory Diaphragm Activity and Pressure Swings Obtained During Quiet Breathing With Zero NAVA and During High NAVA Level*
* 

Data are presented as mean ± SD; au = arbitrary units; XPdi = mean Pdi; NS = not significant.

References

Sinderby, C, Navalesi, P, Beck, J, et al (1999) Neural control of mechanical ventilation.Nat Med5,1433-1436. [PubMed] [CrossRef]
 
Sinderby, C, Beck, J, Weinberg, J, et al Voluntary activation of the human diaphragm in health and disease.J Appl Physiol1998;85,2146-2158. [PubMed]
 
Tremblay, LN, Slutsky, AS Ventilator induced lung injury: from barotrauma to biotrauma.Proc Assoc Am Phys1998;110,482-488. [PubMed]
 
Aldrich, T, Sinderby, C, McKenzie, D, et al Electrophysiologic techniques for the assessment of respiratory muscle function. ATS/ERS statement on respiratory muscle testing.Am J Respir Crit Care Med2002;166,518-624. [PubMed]
 
Sinderby, C, Beck, JC, Lindström, L, et al Enhancement of signal quality in esophageal recordings of diaphragm EMG.J Appl Physiol1997;82,1370-1377. [PubMed]
 
Beck, J, Sinderby, C, Lindström, L, et al Influence of bipolar electrode positioning on measurements of human crural diaphragm EMG.J Appl Physiol1996;81,1434-1449. [PubMed]
 
Beck, J, Sinderby, C, Lindstrom, L, et al Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration.J Appl Physiol1997;82,520-530. [PubMed]
 
Beck, J, Sinderby, C, Lindstrom, L, et al Effects of lung volume on diaphragm EMG signal strength during voluntary contractions.J Appl Physiol1998;85,1123-1134. [PubMed]
 
Sinderby, C, Spahija, J, Beck, J, et al Diaphragm activation during exercise in chronic obstructive pulmonary disease.Am J Respir Crit Care Med2001;163,1637-1641. [PubMed]
 
Sinderby, C, Spahija, J, Beck, J Changes in respiratory effort sensation over time and its link to diaphragm sarcolemma excitability.Am J Respir Crit Care Med2001;163,905-910. [PubMed]
 
Georgopoulos, D, Roussos, C Control of breathing in mechanically ventilated patients.Eur Respir J1996;9,2151-2160. [PubMed]
 
Allo JC, Beck J, Brander L, et al. Influence of neurally adjusted ventilatory assist (NAVA) and PEEP on breathing pattern in rabbits with acute lung injury. Crit Care Med 2006 (in press).
 
Agostoni, E Diaphragm activity and thoracoabdominal mechanics during positive pressure breathing.J Appl Physiol1962;17,215-220. [PubMed]
 
Mills, JN The nature of the limitation of maximal inspiratory and expiratory efforts.J Physiol (Lond)1950;111,376-381. [PubMed]
 
The Acute Respiratory Distress Syndrome Network.. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.N Engl J Med2000;342,1301-1308. [PubMed]
 
Campbell, EJ, Green, JH The variations in intra-abdominal pressure and the activity of the abdominal muscles during breathing; a study in man.J Physiol (Lond)1953;122,282-290. [PubMed]
 
Agostoni, E, Rahn, HJ Abdominal and thoracic pressures at different lung volumes.J Appl Physiol1960;15,1087-1092. [PubMed]
 
Mead, J, Milic-Emili, J, Turner, JM Factors limiting depth of a maximal inspiration in human subjects.J Appl Physiol1963;18,295-296. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543