Neurally adjusted ventilatory assist and proportional assist ventilation both improve patient-ventilator interaction.

INTRODUCTION: The objective was to compare the impact of three assistance levels of different modes of mechanical ventilation; neurally adjusted ventilatory assist (NAVA), proportional assist ventilation (PAV), and pressure support ventilation (PSV) on major features of patient-ventilator interaction. METHODS: PSV, NAVA, and PAV were set to obtain a tidal volume (VT) of 6 to 8 ml/kg (PSV100, NAVA100, and PAV100) in 16 intubated patients. Assistance was further decreased by 50% (PSV50, NAVA50, and PAV50) and then increased by 50% (PSV150, NAVA150, and PAV150) with all modes. The three modes were randomly applied. Airway flow and pressure, electrical activity of the diaphragm (EAdi), and blood gases were measured. VT, peak EAdi, coefficient of variation of VT and EAdi, and the prevalence of the main patient-ventilator asynchronies were calculated. RESULTS: PAV and NAVA prevented the increase of VT with high levels of assistance (median 7.4 (interquartile range (IQR) 5.7 to 10.1) ml/kg and 7.4 (IQR, 5.9 to 10.5) ml/kg with PAV150 and NAVA150 versus 10.9 (IQR, 8.9 to 12.0) ml/kg with PSV150, P <0.05). EAdi was higher with PAV than with PSV at level100 and level150. The coefficient of variation of VT was higher with NAVA and PAV (19 (IQR, 14 to 31)% and 21 (IQR 16 to 29)% with NAVA100 and PAV100 versus 13 (IQR 11 to 18)% with PSV100, P <0.05). The prevalence of ineffective triggering was lower with PAV and NAVA than with PSV (P <0.05), but the prevalence of double triggering was higher with NAVA than with PAV and PSV (P <0.05). CONCLUSIONS: PAV and NAVA both prevent overdistention, improve neuromechanical coupling, restore the variability of the breathing pattern, and decrease patient-ventilator asynchrony in fairly similar ways compared with PSV. Further studies are needed to evaluate the possible clinical benefits of NAVA and PAV on clinical outcomes. TRIAL REGISTRATION: Clinicaltrials.gov NCT02056093 . Registered 18 December 2013.

Neurally adjusted ventilatory assist improves patient-ventilator interaction during postextubation prophylactic noninvasive ventilation.

OBJECTIVES: To compare the respective impact of pressure support ventilation and naturally adjusted ventilatory assist, with and without a noninvasive mechanical ventilation algorithm, on patient-ventilator interaction. DESIGN: Prospective 2-month study. SETTING: Adult critical care unit in a tertiary university hospital. PATIENTS: Seventeen patients receiving a prophylactic postextubation noninvasive mechanical ventilation. INTERVENTIONS: Patients were randomly mechanically ventilated for 10 mins with: pressure support ventilation without a noninvasive mechanical ventilation algorithm (PSV-NIV-), pressure support ventilation with a noninvasive mechanical ventilation algorithm (PSV-NIV+), neurally adjusted ventilatory assist without a noninvasive mechanical ventilation algorithm (NAVA-NIV-), and neurally adjusted ventilatory assist with a noninvasive mechanical ventilation algorithm (NAVA-NIV+). MEASUREMENTS AND MAIN RESULTS: Breathing pattern descriptors, diaphragm electrical activity, leak volume, inspiratory trigger delay, inspiratory time in excess, and the five main asynchronies were quantified. Asynchrony index and asynchrony index influenced by leaks were computed. Peak inspiratory pressure and diaphragm electrical activity were similar for each of the four experimental conditions. For both pressure support ventilation and neurally adjusted ventilatory assist, the noninvasive mechanical ventilation algorithm significantly reduced the level of leakage (p < .01). Inspiratory trigger delay was not affected by the noninvasive mechanical ventilation algorithm but was shorter in neurally adjusted ventilatory assist than in pressure support ventilation (p < .01). Inspiratory time in excess was shorter in neurally adjusted ventilatory assist and PSV-NIV+ than in PSV-NIV- (p < .05). Asynchrony index was not affected by the noninvasive mechanical ventilation algorithm but was significantly lower in neurally adjusted ventilatory assist than in pressure support ventilation (p < .05). Asynchrony index influenced by leaks was insignificant with neurally adjusted ventilatory assist and significantly lower than in pressure support ventilation (p < .05). There was more double triggering with neurally adjusted ventilatory assist. CONCLUSIONS: Both neurally adjusted ventilatory assist and a noninvasive mechanical ventilation algorithm improve patient-ventilator synchrony in different manners. NAVA-NIV+ offers the best compromise between a good patient-ventilator synchrony and a low level of leaks. Clinical studies are required to assess the potential clinical benefit of neurally adjusted ventilatory assist in patients receiving noninvasive mechanical ventilation. TRIAL REGISTRATION: Clinicaltrials.gov Identifier NCT01280760.

Adjusting ventilator settings to relieve dyspnoea modifies brain activity in critically ill patients: an electroencephalogram pilot study.

Dyspnoea is frequent and distressing in patients receiving mechanical ventilation, but it is often not properly evaluated by caregivers. Electroencephalographic signatures of dyspnoea have been identified experimentally in healthy subjects. We hypothesized that adjusting ventilator settings to relieve dyspnoea in MV patients would induce EEG changes. This was a first-of-its-kind observational study in a convenience population of 12 dyspnoeic, mechanically ventilated patients for whom a decision to adjust the ventilator settings was taken by the physician in charge (adjustments of pressure support, slope, or trigger). Pre- and post-ventilator adjustment electroencephalogram recordings were processed using covariance matrix statistical classifiers and pre-inspiratory potentials. The pre-ventilator adjustment median dyspnoea visual analogue scale was 3.0 (interquartile range: 2.5-4.0; minimum-maximum: 1-5) and decreased by (median) 3.0 post-ventilator adjustment. Statistical classifiers adequately detected electroencephalographic changes in 8 cases (area under the curve ≥0.7). Previously present pre-inspiratory potentials disappeared in 7 cases post-ventilator adjustment. Dyspnoea improvement was consistent with electroencephalographic changes in 9 cases. Adjusting ventilator settings to relieve dyspnoea produced detectable changes in brain activity. This paves the way for studies aimed at determining whether monitoring respiratory-related electroencephalographic activity can improve outcomes in critically ill patients under mechanical ventilation.

Expiratory load compensation is associated with electroencephalographic premotor potentials in humans.

In normal humans during quiet breathing, expiration is mostly driven by elastic recoil of the lungs. Expiration becomes active when ventilation must be increased to meet augmented metabolic demands, or in response to expiratory loading, be it experimental or disease-related. The response to expiratory loading is considered to be mediated by both reflex and cortical mechanisms, but the latter phenomenon have not been neurophysiologically characterized. We recorded the EEG in 20 healthy volunteers (9 men, 11 women, age: 22 to 50 yr) during unloaded breathing, voluntary expirations, and in response to 50 cmH2O·l(-1)·s expiratory resistive load (ERL), 20 cmH2O expiratory threshold load (high ETL), and 10 cmH2O expiratory threshold load (low ETL). EEGs were processed by ensemble averaging expiratory time-locked segments and examined for pre-expiratory potentials, defined as a slow negative shift from the baseline signal preceding expiration, and suggestive of cortical preparation of expiration involving the supplementary motor area. Four subjects were excluded because of technical EEG problems. Pre-expiratory potentials were present in one subject at baseline and in all subjects during voluntary expirations. They were present in eight subjects during low ETL, in 15 subjects during high ETL, and in 13 subjets during ERL (control vs. low ETL, P = 0.008; control vs. high ETL, P < 0.001; and control vs. ERL, P < 0.001). Respiratory discomfort was more intense in the presence of pre-expiratory potentials (P < 0.001). These results provide a neurophysiological substrate to a cortical component of the physiological response to experimental expiratory loads in humans.

Dyspnea and surface inspiratory electromyograms in mechanically ventilated patients.

CONTEXT: Pressure support ventilation (PSV) must be tailored to the load capacity balance of the respiratory system. While "over assistance" generated hyperinflation and ineffective efforts, "under assistance" increased respiratory drive and causes dyspnea. Surface electromyograms (sEMGs) of extradiaphragmatic inspiratory muscles were responsive to respiratory loading/unloading. OBJECTIVES: To determine if sEMGs of extradiaphragmatic inspiratory muscles vary with PSV settings and relate to the degree of discomfort and the intensity of dyspnea in acutely ill patients. DESIGN: Pathophysiological study, prospective inclusions of 12 intubated adult patients. INTERVENTIONS: Two PSV levels (high and low) and two expiratory trigger (ET) levels (high and low). MEASUREMENTS: Surface electromyograms of the scalene, parasternal, and Alae Nasi muscles (peak, EMGmax; area under the curve, EMGAUC); dyspnea visual analogue scale (VAS); prevalence of ineffective triggering efforts. MAIN RESULTS: For the three recorded muscles, EMGmax and EMGAUC were significantly greater with low PS than high PS. The influence of ET was less important. A strong correlation was found between dyspnea and EMGmax. A significant inverse correlation was found between the prevalence of ineffective efforts and both dyspnea-VAS and EMGmin. CONCLUSIONS: Surface electromyograms of extradiaphragmatic inspiratory muscles provides a simple, reliable and non-invasive indicator of respiratory muscle loading/unloading in mechanically ventilated patients. Because this EMG activity is strongly correlated to the intensity of dyspnea, it could be used as a surrogate of respiratory sensations in mechanically ventilated patients, and might, therefore, provide a monitoring tool in patients in whom detection and quantification of dyspnea is complex if not impossible.

Functional magnetic resonance imaging suggests automatization of the cortical response to inspiratory threshold loading in humans.

Inspiratory threshold loading (ITL) induces cortical activation. It is sustained over time and is resistant to distraction, suggesting automaticity. We hypothesized that ITL-induced changes in cerebral activation may differ between single-breath ITL and continuous ITL, with differences resembling those observed after cortical automatization of motor tasks. We analyzed the brain blood oxygen level dependent (BOLD) signal of 11 naive healthy volunteers during 5 min of random, single-breath ITL and 5 min of continuous ITL. Single-breath ITL increased BOLD in many areas (premotor cortices, bilateral insula, cerebellum, reticular formation of the lateral mesencephalon) and decreased BOLD in regions co-localizing with the default mode network. Continuous ITL induced signal changes in a limited number of areas (supplementary motor area). These differences are comparable to those observed before and after overlearning of motor tasks. We conclude that the respiratory-related cortical activation observed in response to ITL is likely due to automated, attention-independent mechanisms. Also, ITL activates cortical circuits right from the first breath.

Dyspnea-pain counterirritation induced by inspiratory threshold loading: a laser-evoked potentials study.

BACKGROUND: experimentally induced dyspnea of the work/effort type inhibits, in a top-down manner, the spinal transmission of nociceptive inputs (dyspnea-pain counterirritation). Previous studies have demonstrated that this inhibition can be assessed by measuring the nociceptive flexion reflex (RIII). However, its clinical application is limited because of the strong discomfort associated with the electrical stimuli required to elicit the RIII reflex. STUDY OBJECTIVES: we examined whether the dyspnea-pain counterirritation phenomenon can be evaluated by measuring the effect of work/effort type dyspnea on the magnitude of laser-evoked brain potentials (LEPs). METHODS: 10 normal male volunteers were studied (age: 19-30 years). LEPs were elicited using a CO(2) laser stimulator delivering 10- to 15-ms stimuli of 6 ± 0.7 W over a 12.5 mm(2) area. The EEG was recorded using nine scalp channels. Non-nociceptive somatosensory-evoked potentials (SEPs) served as control. LEPs and SEPs were recorded before, during, and after 10 min of experimentally induced dyspnea [inspiratory threshold loading (ITL)]. RESULTS: pain caused by the nociceptive laser stimulus was mild. ITL consistently induced dyspnea, mostly of the "excessive effort" type. Amplitude of the N2-P2 wave of LEPs decreased by 37.6 ± 13.8% during ITL and was significantly correlated with the intensity of dyspnea [r = 0.66, CI 95% (0.08-0.92, P = 0.0319)]. In contrast, ITL had no effect on the magnitude of non-nociceptive SEPs. DISCUSSION: experimentally induced dyspnea of the work/effort type reduces the magnitude of LEPs. This reduction correlates with the intensity of dyspnea. The recording of LEPs could constitute a clinically applicable approach to assess the dyspnea-pain counterirritation phenomenon in patients.