Expiratory Muscle Activity Counteracts Positive End-Expiratory Pressure and Is Associated with Fentanyl Dose in Patients with Acute Respiratory Distress Syndrome.

Rationale: Hypoxemia during mechanical ventilation might be worsened by expiratory muscle activity, which reduces end-expiratory lung volume through lung collapse. A proposed mechanism of benefit of neuromuscular blockade in acute respiratory distress syndrome (ARDS) is the abolition of expiratory efforts. This may contribute to the restoration of lung volumes. The prevalence of this phenomenon, however, is unknown. Objectives: To investigate the incidence and amount of end-expiratory lung impedance (EELI) increase after the administration of neuromuscular blocking agents (NMBAs), clinical factors associated with this phenomenon, its impact on regional lung ventilation, and any association with changes in pleural pressure. Methods: We included mechanically ventilated patients with ARDS monitored with electrical impedance tomography (EIT) who received NMBAs in one of two centers. We measured changes in EELI, a surrogate for end-expiratory lung volume, before and after NMBA administration. In an additional 10 patients, we investigated the characteristic signatures of expiratory muscle activity depicted by EIT and esophageal catheters simultaneously. Clinical factors associated with EELI changes were assessed. Measurements and Main Results: We included 46 patients, half of whom showed an increase in EELI of >10% of the corresponding Vt (46.2%; IQR, 23.9-60.9%). The degree of EELI increase correlated positively with fentanyl dosage and negatively with changes in end-expiratory pleural pressures. This suggests that expiratory muscle activity might exert strong counter-effects against positive end-expiratory pressure that are possibly aggravated by fentanyl. Conclusions: Administration of NMBAs during EIT monitoring revealed activity of expiratory muscles in half of patients with ARDS. The resultant increase in EELI had a dose-response relationship with fentanyl dosage. This suggests a potential side effect of fentanyl during protective ventilation.

Effect of Cardiogenic Oscillations on Trigger Delay During Pressure Support Ventilation.

BACKGROUND: Sensitive flow or pressure triggers are usually applied to improve ventilator response time. Conversely, too sensitive triggers can incur risk of auto-triggering, a type of asynchrony in which a breath is triggered without inspiratory muscle activity. A frequent cause of auto-triggering is cardiogenic oscillations, characterized by cyclical variations in pressure and flow waveforms caused by cardiac contractions. Our goal was to test trigger performance and capacity to abolish auto-triggering in 5 different ICU ventilators using different simulated levels of cardiogenic oscillations. METHODS: A mechanical breathing simulator was used to test 5 different ICU ventilators' trigger response time and capacity to minimize auto-triggering in conditions with 0, 0.25, 0.5, and 1 cm H2O cardiogenic oscillation. Each ventilator was evaluated until an ideal trigger was found (the most sensitive that abolished auto-triggering). When the least sensitive flow trigger was unable to avoid auto-triggering, a pressure trigger was used. We compared time delay, airway pressure drop until triggering, and work of breathing before each trigger, all at the ideal trigger level for each cardiogenic oscillation amplitude. We also assessed the proportion of auto-triggered breaths in the whole range of trigger levels tested. RESULTS: Larger cardiogenic oscillations were associated with more frequent auto-triggering. To avoid auto-triggering, less sensitive triggers were required (+2.51 L/min per 1 cm H2O increase in cardiogenic oscillation; 95% CI 2.26-2.76, P < .001). Time delay increased with larger cardiogenic oscillations, because less sensitive trigger levels were required to abolish auto-triggering (4.79-ms increase per 1 L/min increment on flow trigger). CONCLUSIONS: More sensitive triggers led to faster ventilator response, but also to more frequent auto-triggering. To avoid auto-triggering, less sensitive triggers were required, with consequent slower trigger response. To compare trigger performance in a scenario that more closely represents clinical practice, evaluation of the tradeoff between time delay and frequency of auto-triggering should be considered.

High Positive End-Expiratory Pressure Renders Spontaneous Effort Noninjurious.

RATIONALE: In acute respiratory distress syndrome (ARDS), atelectatic solid-like lung tissue impairs transmission of negative swings in pleural pressure (Ppl) that result from diaphragmatic contraction. The localization of more negative Ppl proportionally increases dependent lung stretch by drawing gas either from other lung regions (e.g., nondependent lung [pendelluft]) or from the ventilator. Lowering the level of spontaneous effort and/or converting solid-like to fluid-like lung might render spontaneous effort noninjurious. OBJECTIVES: To determine whether spontaneous effort increases dependent lung injury, and whether such injury would be reduced by recruiting atelectatic solid-like lung with positive end-expiratory pressure (PEEP). METHODS: Established models of severe ARDS (rabbit, pig) were used. Regional histology (rabbit), inflammation (positron emission tomography; pig), regional inspiratory Ppl (intrabronchial balloon manometry), and stretch (electrical impedance tomography; pig) were measured. Respiratory drive was evaluated in 11 patients with ARDS. MEASUREMENTS AND MAIN RESULTS: Although injury during muscle paralysis was predominantly in nondependent and middle lung regions at low (vs. high) PEEP, strong inspiratory effort increased injury (indicated by positron emission tomography and histology) in dependent lung. Stronger effort (vs. muscle paralysis) caused local overstretch and greater tidal recruitment in dependent lung, where more negative Ppl was localized and greater stretch was generated. In contrast, high PEEP minimized lung injury by more uniformly distributing negative Ppl, and lowering the magnitude of spontaneous effort (i.e., deflection in esophageal pressure observed in rabbits, pigs, and patients). CONCLUSIONS: Strong effort increased dependent lung injury, where higher local lung stress and stretch was generated; effort-dependent lung injury was minimized by high PEEP in severe ARDS, which may offset need for paralysis.