Neurally adjusted ventilatory assist in patients with critical illness-associated polyneuromyopathy

Purpose: Diaphragmatic electrical activity (EAdi), 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 aw) in proportion to EAdi, 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 72h. Changes in tidal volume (V t) generation per unit of EAdi (V t/EAdi) 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 EAdi amplitude was 9.0 (4.4-15.2)μV, and the V t was 6.5 (3.7-14.3)ml/kg predicted body weight. V t, respiratory rate, EAdi, PaCO2, and hemodynamic parameters remained unchanged, while PaO2/FiO2 increased from 238 (121-337) to 282 (150-440)mmHg (p=0.007) during NAVAal. V t/EAdi 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, EAdi and its feedback control are sufficiently preserved to titrate and implement NAVA for up to 3days. Whether monitoring neuro-ventilatory efficiency helps inform the weaning process warrants further evaluatio

Subject–ventilator synchrony during neural versus pneumatically triggered non-invasive helmet ventilation

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

NEURAL CONTROL OF VENTILATION PREVENTS BOTH OVER-DISTENSION AND DE-RECRUITMENT OF EXPERIMENTALLY INJURED LUNGS.

BACKGROUND Endogenous pulmonary reflexes may protect the lungs during mechanical ventilation. We aimed to assess integration of continuous neurally adjusted ventilatory assist (cNAVA), delivering assist in proportion to diaphragm's electrical activity during inspiration and expiration, and Hering-Breuer inflation and deflation reflexes on lung recruitment, distension, and aeration before and after acute lung injury (ALI). METHODS In 7 anesthetised rabbits with bilateral pneumothoraces, we identified adequate cNAVA level (cNAVAAL) at the plateau in peak ventilator pressure during titration procedures before (healthy lungs with endotracheal tube, [HLETT]) and after ALI (endotracheal tube [ALIETT] and during non-invasive ventilation [ALINIV]). Following titration, cNAVAAL was maintained for 5minutes. In 2 rabbits, procedures were repeated after vagotomy (ALIETT+VAG). In 3 rabbits delivery of assist was temporarily modulated to provide assist on inspiration only. Computed tomography was performed before intubation, before ALI, during cNAVA titration, and after maintenance at cNAVAAL. RESULTS During ALIETT and ALINIV, normally aerated lung-regions doubled and poorly aerated lung-regions decreased to less than a third (p<0.05) compared to HLETT; no over-distension was observed. Tidal volumes were<5ml/kg throughout. Removing assist during expiration resulted in lung de-recruitment during ALIETT, but not during ALINIV. During ALIETT+VAG the expiratory portion of EAdi disappeared, resulting in cyclic lung collapse and recruitment. CONCLUSIONS When using cNAVA in ALI, vagally mediated reflexes regulated lung recruitment preventing both lung over-distension and atelectasis. During non-invasive cNAVA the upper airway muscles play a role in preventing atelectasis. Future studies should be performed to compare these findings with conventional lung-protective approaches

The calcium sensitizer levosimendan improves human diaphragm function.

Contains fulltext : 109764.pdf (publisher's version ) (Open Access)RATIONALE: Acquired diaphragm muscle weakness is a key feature in several chronic conditions, including chronic obstructive pulmonary disease, congestive heart failure, and difficult weaning from mechanical ventilation. No drugs are available to improve respiratory muscle function in these patients. Recently, we have shown that the calcium sensitizer levosimendan enhances the force-generating capacity of isolated diaphragm fibers. OBJECTIVES: To investigate the effects of the calcium sensitizer levosimendan on in vivo human diaphragm function. METHODS: In a double-blind, randomized, crossover design, 30 healthy subjects performed two identical inspiratory loading tasks. After the first loading task, subjects received levosimendan (40 mug/kg bolus followed by 0.1/0.2 mug/kg/min continuous infusion) or placebo. Transdiaphragmatic pressure, diaphragm electrical activity, and their relationship (neuromechanical efficiency) were measured during loading. Magnetic phrenic nerve stimulation was performed before the first loading task and after bolus administration to assess twitch contractility. Center frequency of diaphragm electrical activity was evaluated to study the effects of levosimendan on muscle fiber conduction velocity. MEASUREMENTS AND MAIN RESULTS: The placebo group showed a 9% (P=0.01) loss of twitch contractility after loaded breathing, whereas no loss in contractility was observed in the levosimendan group. Neuro-mechanical efficiency of the diaphragm during loading improved by 21% (P<0.05) in the levosimendan group. Baseline center frequency of diaphragm electrical activity was reduced after levosimendan administration (P<0.05). CONCLUSIONS: The calcium sensitizer levosimendan improves neuromechanical efficiency and contractile function of the human diaphragm. Our findings suggest a new therapeutic approach to improve respiratory muscle function in patients with respiratory failure

Heart-lung interactions during neurally adjusted ventilatory assist

Introduction Assist in unison to the patient’s inspiratory neural effort and feedback-controlled limitation of lung distension with neurally adjusted ventilatory assist (NAVA) may reduce the negative effects of mechanical ventilation on right ventricular function. Methods Heart–lung interaction was evaluated in 10 intubated patients with impaired cardiac function using esophageal balloons, pulmonary artery catheters and echocardiography. Adequate NAVA level identified by a titration procedure to breathing pattern (NAVAal), 50% NAVAal, and 200% NAVAal and adequate pressure support (PSVal, defined clinically), 50% PSVal, and 150% PSVal were implemented at constant positive end-expiratory pressure for 20 minutes each. Results NAVAal was 3.1 ± 1.1cmH2O/μV and PSVal was 17 ± 2 cmH20. For all NAVA levels negative esophageal pressure deflections were observed during inspiration whereas this pattern was reversed during PSVal and PSVhigh. As compared to expiration, inspiratory right ventricular outflow tract velocity time integral (surrogating stroke volume) was 103 ± 4%, 109 ± 5%, and 100 ± 4% for NAVAlow, NAVAal, and NAVAhigh and 101 ± 3%, 89 ± 6%, and 83 ± 9% for PSVlow, PSVal, and PSVhigh, respectively (p < 0.001 level-mode interaction, ANOVA). Right ventricular systolic isovolumetric pressure increased from 11.0 ± 4.6 mmHg at PSVlow to 14.0 ± 4.6 mmHg at PSVhigh but remained unchanged (11.5 ± 4.7 mmHg (NAVAlow) and 10.8 ± 4.2 mmHg (NAVAhigh), level-mode interaction p = 0.005). Both indicate progressive right ventricular outflow impedance with increasing pressure support ventilation (PSV), but no change with increasing NAVA level. Conclusions Right ventricular performance is less impaired during NAVA compared to PSV as used in this study. Proposed mechanisms are preservation of cyclic intrathoracic pressure changes characteristic of spontaneous breathing and limitation of right-ventricular outflow impedance during inspiration, regardless of the NAVA level

Heart–lung interactions during neurally adjusted ventilatory assist

Abstract Introduction Assist in unison to the patient’s inspiratory neural effort and feedback-controlled limitation of lung distension with neurally adjusted ventilatory assist (NAVA) may reduce the negative effects of mechanical ventilation on right ventricular function. Methods Heart–lung interaction was evaluated in 10 intubated patients with impaired cardiac function using esophageal balloons, pulmonary artery catheters and echocardiography. Adequate NAVA level identified by a titration procedure to breathing pattern (NAVAal), 50% NAVAal, and 200% NAVAal and adequate pressure support (PSVal, defined clinically), 50% PSVal, and 150% PSVal were implemented at constant positive end-expiratory pressure for 20 minutes each. Results NAVAal was 3.1 ± 1.1cmH2O/μV and PSVal was 17 ± 2 cmH20. For all NAVA levels negative esophageal pressure deflections were observed during inspiration whereas this pattern was reversed during PSVal and PSVhigh. As compared to expiration, inspiratory right ventricular outflow tract velocity time integral (surrogating stroke volume) was 103 ± 4%, 109 ± 5%, and 100 ± 4% for NAVAlow, NAVAal, and NAVAhigh and 101 ± 3%, 89 ± 6%, and 83 ± 9% for PSVlow, PSVal, and PSVhigh, respectively (p < 0.001 level-mode interaction, ANOVA). Right ventricular systolic isovolumetric pressure increased from 11.0 ± 4.6 mmHg at PSVlow to 14.0 ± 4.6 mmHg at PSVhigh but remained unchanged (11.5 ± 4.7 mmHg (NAVAlow) and 10.8 ± 4.2 mmHg (NAVAhigh), level-mode interaction p = 0.005). Both indicate progressive right ventricular outflow impedance with increasing pressure support ventilation (PSV), but no change with increasing NAVA level. Conclusions Right ventricular performance is less impaired during NAVA compared to PSV as used in this study. Proposed mechanisms are preservation of cyclic intrathoracic pressure changes characteristic of spontaneous breathing and limitation of right-ventricular outflow impedance during inspiration, regardless of the NAVA level. Trial registration Clinicaltrials.gov Identifier: NCT00647361, registered 19 March 200