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Background: We previously showed in animals that transpulmonary driving pressure (PL) can be estimated during Neurally Adjusted Ventilatory Assist (NAVA) and Neural Pressure Support (NPS) using a single lower assist maneuver (LAM). The aim of this study was to test the LAM-based estimate of PL (PL_LAM) in patients with acute respiratory failure. Methods: This was a prospective, physiological, and interventional study in intubated patients with acute respiratory failure. During both NAVA and simulated NPS (high and low levels of assist), a LAM was performed every 3 min by manually reducing the assist to zero for one single breath (by default, ventilator still provides 2 cmH2O). Following NAVA and NPSSIM periods, patients were sedated and passively ventilated in volume control and pressure control ventilation, to obtain PL during controlled mechanical ventilation (PL_CMV). PL using an esophageal balloon (PL_Pes) was also compared to PL_LAM and PL_CMV. We measured diaphragm electrical activity (Edi), ventilator pressure (PVent), esophageal pressure (Pes) and tidal volume. PL_LAM and PL_Pes were compared to themselves, and to PL_CMV for matching flows and volumes. Results: Ten patients were included in the study. For the group, PL_LAM was closely similar to PL_CMV, with a high correlation (R2 = 0.88). Bland–Altman analysis revealed a low Bias of 0.28 cmH2O, and 1.96SD of 5.26 cmH2O. PL_LAM vs PL_Pes were also tightly related (R2 = 0.77). Conclusion: This physiological study in patients confirms our previous pre-clinical data that PL_LAM is as good an estimate as PL_Pes to determine PL, in spontaneously breathing patients on assisted mechanical ventilation. Trial registration The study was registered at clinicaltrials.gov (ID NCT05378802) on November 6, 2021 [ABSTRACT FROM AUTHOR]

Background: The unsuccessful extubation in patients with traumatic cervical spinal cord injuries (CSCI) may result from impairment diaphragm function and monitoring of diaphragm electrical activity (EAdi) can be informative in guiding extubation. We aimed to evaluate whether the change of EAdi during a single maximal maneuver can predict extubation outcomes in CSCI patients. Methods: This is a retrospective study of CSCI patients requiring mechanical ventilation in the ICU of a tertiary hospital. A single maximal maneuver was performed by asking each patient to inhale with maximum strength during the first spontaneous breathing trial (SBT). The baseline (during SBT before maximal maneuver), maximum (during the single maximal maneuver), and the increase of EAdi (ΔEAdi, equal to the difference between baseline and maximal) were measured. The primary outcome was extubation success, defined as no reintubation after the first extubation and no tracheostomy before any extubation during the ICU stay. Results: Among 107 patients enrolled, 50 (46.7%) were extubated successfully at the first SBT. Baseline EAdi, maximum EAdi, and ΔEAdi were significantly higher, and the rapid shallow breathing index was lower in patients who were extubated successfully than in those who failed. By multivariable logistic analysis, ΔEAdi was independently associated with successful extubation (OR 2.03, 95% CI 1.52–3.17). ΔEAdi demonstrated high diagnostic accuracy in predicting extubation success with an AUROC 0.978 (95% CI 0.941–0.995), and the cut-off value was 7.0 μV. Conclusions: The increase of EAdi from baseline SBT during a single maximal maneuver is associated with successful extubation and can help guide extubation in CSCI patients. [ABSTRACT FROM AUTHOR]

Purpose: Respiratory muscle weakness frequently develops in critically ill patients and is associated with adverse outcome, including difficult weaning from mechanical ventilation. Today, no drug is approved to improve respiratory muscle function in these patients. Previously, we have shown that the calcium sensitizer levosimendan improves calcium sensitivity of human diaphragm muscle fibers in vitro and contractile efficiency of the diaphragm in healthy subjects. The main purpose of this study is to investigate the effects of levosimendan on diaphragm contractile efficiency in mechanically ventilated patients.Methods: In a double-blind randomized placebo-controlled trial, mechanically ventilated patients performed two 30-min continuous positive airway pressure (CPAP) trials with 5-h interval. After the first CPAP trial, study medication (levosimendan 0.2 µg/kg/min continuous infusion or placebo) was administered. During the CPAP trials, electrical activity of the diaphragm (EAdi), transdiaphragmatic pressure (Pdi), and flow were measured. Neuromechanical efficiency (primary outcome parameter) was calculated.Results: Thirty-nine patients were included in the study. Neuromechanical efficiency was not different during the CPAP trial after levosimendan administration compared to the CPAP trial before study medication. Tidal volume and minute ventilation were higher after levosimendan administration (11 and 21%, respectively), whereas EAdi and Pdi were higher in both groups in the CPAP trial after study medication compared to the CPAP trial before study medication.Conclusions: Levosimendan does not improve diaphragm contractile efficiency. [ABSTRACT FROM AUTHOR]

Background: We aimed (1) to describe the characteristics of patient-ventilator asynchrony in a population of critically ill children, (2) to describe the risk factors associated with patient-ventilator asynchrony, and (3) to evaluate the association between patient-ventilator asynchrony and ventilator-free days at day 28. Methods: In this single-center prospective study, consecutive children admitted to the PICU and mechanically ventilated for at least 24 h were included. Patient-ventilator asynchrony was analyzed by comparing the ventilator pressure curve and the electrical activity of the diaphragm (Edi) signal with (1) a manual analysis and (2) using a standardized fully automated method. Results: Fifty-two patients (median age 6 months) were included in the analysis. Eighteen patients had a very low ventilatory drive (i.e., peak Edi < 2 µV on average), which prevented the calculation of patient-ventilator asynchrony. Children spent 27% (interquartile 22-39%) of the time in conflict with the ventilator. Cycling-off errors and trigger delays contributed to most of this asynchronous time. The automatic algorithm provided a NeuroSync index of 45%, confirming the high prevalence of asynchrony. No association between the severity of asynchrony and ventilator-free days at day 28 or any other clinical secondary outcomes was observed, but the proportion of children with good synchrony was very low. Conclusion: Patient-ventilator interaction is poor in children supported by conventional ventilation, with a high frequency of depressed ventilatory drive and a large proportion of time spent in asynchrony. The clinical benefit of strategies to improve patient-ventilator interactions should be evaluated in pediatric critical care. [ABSTRACT FROM AUTHOR]

A letter to the editor and a reply to the article about a study which investigates the clinical outcome of complementary modes of mechanical ventilation in a 2016 issue is presented.

Purpose: During neurally adjusted ventilatory assist (NAVA), it is difficult to quantify the relative contribution of the patient versus the ventilator to the inspiratory tidal volume (Vt). To solve this problem, we developed an index, the 'patient-ventilator breath contribution' (PVBC), using the inspiratory deflection of the diaphragmatic electrical activity (∆EAdi) and Vt during assisted and non-assisted breaths. This study evaluated the PVBC index in an experimental setup. Method: Nine intubated and sedated rabbits were studied during repeated ramp increases of the NAVA level. One breath was non-assisted at each NAVA level. The PVBC index was evaluated during resistive loading and after acute lung injury. PVBC was calculated by relating Vt/∆EAdi of a non-assisted breath to that of the preceding assisted breath. The PVBC was compared to the relative contribution of esophageal pressure (∆Pes) to transpulmonary pressure deflections (∆ P). Results: The relationship between PVBC and ∆Pes/∆ P was slightly curvilinear with an intercept different from zero ( y = −1 x+ 1.64 x + 0.21) and a determination coefficient ( R) of 0.95. Squaring the PVBC values resulted in a near perfect linear relationship ( y = 1.02 x + 0.05) between PVBC and ∆Pes/∆ P with an R of 0.97. Conclusion: This study shows that Vt and EAdi can be used to predict the contribution of the inspiratory muscles versus that of the ventilator during NAVA. If clinically applicable, this could serve to quantify and standardize the adjustment of the level of assist, and hence reduce the risks of excessive ventilatory assist. Further studies are required to evaluate if this method is clinically applicable. [ABSTRACT FROM AUTHOR]

Purpose: Diaphragmatic electrical activity (EA), reflecting respiratory drive, and its feedback control might be impaired in critical illness-associated polyneuromyopathy (CIPM). We aimed to evaluate whether titration and prolonged application of neurally adjusted ventilatory assist (NAVA), which delivers pressure ( P) in proportion to EA, is feasible in CIPM patients. Methods: Peripheral and phrenic nerve electrophysiology studies were performed in 15 patients with clinically suspected CIPM and in 14 healthy volunteers. In patients, an adequate NAVA level (NAVAal) was titrated daily and was implemented for a maximum of 72 h. Changes in tidal volume ( V) generation per unit of EA ( V/EA) were assessed daily during standardized tests of neuro-ventilatory efficiency (NVET). Results: In patients (median [range], 66 [44-80] years), peripheral electrophysiology studies confirmed CIPM. Phrenic nerve latency (PNL) was prolonged and diaphragm compound muscle action potential (CMAP) was reduced compared with healthy volunteers ( p < 0.05 for both). NAVAal could be titrated in all but two patients. During implementation of NAVAal for 61 (37-64) h, the EA amplitude was 9.0 (4.4-15.2) μV, and the V was 6.5 (3.7-14.3) ml/kg predicted body weight. V, respiratory rate, EA, PaCO, and hemodynamic parameters remained unchanged, while PaO/FiO increased from 238 (121-337) to 282 (150-440) mmHg ( p = 0.007) during NAVAal. V/EA changed by −10 (−46; +31)% during the first NVET and by −0.1 (−26; +77)% during the last NVET ( p = 0.048). Conclusion: In most patients with CIPM, EA and its feedback control are sufficiently preserved to titrate and implement NAVA for up to 3 days. Whether monitoring neuro-ventilatory efficiency helps inform the weaning process warrants further evaluation. [ABSTRACT FROM AUTHOR]

To determine if neurally adjusted ventilatory assist (NAVA) that delivers pressure in proportion to diaphragm electrical activity is as protective to acutely injured lungs (ALI) and non-pulmonary organs as volume controlled (VC), low tidal volume (Vt), high positive end-expiratory pressure (PEEP) ventilation. Prospective, randomized, laboratory animal study. Twenty-seven male New Zealand white rabbits. Anesthetized rabbits with hydrochloric acid-induced ALI were randomized ( n = 9 per group) to 5.5 h NAVA (non-paralyzed), VC (paralyzed; Vt 6-ml/kg), or VC (paralyzed; Vt 15-ml/kg). PEEP was adjusted to hemodynamic goals in NAVA and VC6-ml/kg, and was 1 cmH2O in VC15-ml/kg. PaO2/FiO2; lung wet-to-dry ratio; lung histology; interleukin-8 (IL-8) concentrations in broncho-alveolar-lavage (BAL) fluid, plasma, and non-pulmonary organs; plasminogen activator inhibitor type-1 and tissue factor in BAL fluid and plasma; non-pulmonary organ apoptosis rate; creatinine clearance; echocardiography. PEEP was similar in NAVA and VC6-ml/kg. During NAVA, Vt was lower (3.1 ± 0.9 ml/kg), whereas PaO2/FiO2, respiratory rate, and PaCO2 were higher compared to VC6-ml/kg ( p < 0.05 for all). Variables assessing ventilator-induced lung injury (VILI), IL-8 levels, non-pulmonary organ apoptosis rate, and kidney as well as cardiac performance were similar in NAVA compared to VC6-ml/kg. VILI and non-pulmonary organ dysfunction was attenuated in both groups compared to VC15-ml/kg. In anesthetized rabbits with early experimental ALI, NAVA is as effective as VC6-ml/kg in preventing VILI, in attenuating excessive systemic and remote organ inflammation, and in preserving cardiac and kidney function. [ABSTRACT FROM AUTHOR]

Objective: Patient-ventilator synchrony during non-invasive pressure support ventilation with the helmet device is often compromised when conventional pneumatic triggering and cycling-off were used. A possible solution to this shortcoming is to replace the pneumatic triggering with neural triggering and cycling-off-using the diaphragm electrical activity (EA(di)). This signal is insensitive to leaks and to the compliance of the ventilator circuit.Design: Randomized, single-blinded, experimental study.Setting: University Hospital. PARTICIPANTS AND SUBJECTS: Seven healthy human volunteers.Interventions: Pneumatic triggering and cycling-off were compared to neural triggering and cycling-off during NIV delivered with the helmet.Measurements and Results: Triggering and cycling-off delays, wasted efforts, and breathing comfort were determined during restricted breathing efforts (<20% of voluntary maximum EA(di)) with various combinations of pressure support (PSV) (5, 10, 20 cm H(2)O) and respiratory rates (10, 20, 30 breath/min). During pneumatic triggering and cycling-off, the subject-ventilator synchrony was progressively more impaired with increasing respiratory rate and levels of PSV (p < 0.001). During neural triggering and cycling-off, effect of increasing respiratory rate and levels of PSV on subject-ventilator synchrony was minimal. Breathing comfort was higher during neural triggering than during pneumatic triggering (p < 0.001).Conclusions: The present study demonstrates in healthy subjects that subject-ventilator synchrony, trigger effort, and breathing comfort with a helmet interface are considerably less impaired during increasing levels of PSV and respiratory rates with neural triggering and cycling-off, compared to conventional pneumatic triggering and cycling-off. [ABSTRACT FROM AUTHOR]

Neurally adjusted ventilatory assist uses the electrical activity of the diaphragm (EAdi)—a pneumatically-independent signal—to control the timing and pressure of the ventilation delivered, and should not be affected by leaks. The aim of this study was to evaluate whether NAVA can deliver assist in synchrony and proportionally to EAdi after extubation, with a leaky non-invasive interface. Prospective, controlled experimental study in an animal laboratory. Ten rabbits, anesthetized, mechanically ventilated. Following lung injury, the following was performed in sequential order: (1) NAVA delivered via oral endotracheal tube with PEEP; (2) same as (1) without PEEP; (3) non-invasive NAVA at unchanged NAVA level and no PEEP via a single nasal prong; (4) no assist; (5) non-invasive NAVA at progressively increasing NAVA levels. EAdi, esophageal pressure, blood gases and hemodynamics were measured during each condition. For the same NAVA level, the mean delivered pressure above PEEP increased from 3.9 ± 1.4 cmH2O (intubated) to 7.5 ± 3.8 cmH2O (non-invasive) ( p < 0.05) because of increased EAdi. No changes were observed in PaO2 and PaCO2. Increasing the NAVA level fourfold during non-invasive NAVA restored EAdi and esophageal pressure swings to pre-extubation levels. Triggering (106 ± 20 ms) and cycling-off delays (40 ± 21 ms) during intubation were minimal and not worsened by the leak (95 ± 13 ms and 33 ± 9 ms, respectively). NAVA can be effective in delivering non-invasive ventilation even when the interface with the patient is excessively leaky, and can unload the respiratory muscles while maintaining synchrony with the subject's demand. [ABSTRACT FROM AUTHOR]

Investigates the neural control of mechanical ventilation in respiratory failure. Neural control of ventilatory assist; Methods for controlling partial ventilatory support; Neural triggering; Neurally adjusted ventilatory assist.