Comparing the Effects of Tidal Volume, Driving Pressure, and Mechanical Power on Mortality in Trials of Lung-Protective Mechanical Ventilation.

BACKGROUND: The unifying goal of lung-protective ventilation strategies in ARDS is to minimize the strain and stress applied by mechanical ventilation to the lung to reduce ventilator-induced lung injury (VILI). The relative contributions of the magnitude and frequency of mechanical stress and the end-expiratory pressure to the development of VILI is unknown. Consequently, it is uncertain whether the risk of VILI is best quantified in terms of tidal volume (VT), driving pressure (ΔP), or mechanical power. METHODS: The correlation between differences in VT, ΔP, and mechanical power and the magnitude of mortality benefit in trials of lung-protective ventilation strategies in adult subjects with ARDS was assessed by meta-regression. Modified mechanical power was computed including PEEP (Powerelastic), excluding PEEP (Powerdynamic), and using ΔP (Powerdriving). The primary analysis incorporated all included trials. A secondary subgroup analysis was restricted to trials of lower versus higher PEEP strategies. RESULTS: We included 9 trials involving 4,731 subjects in the analysis. Odds ratios for moderation derived from meta-regression showed that variations in VT, ΔP, and Powerdynamic were associated with increased mortality with odds ratios of 1.24 (95% CI 1.03-1.49), 1.31 (95% CI 1.03-1.66), and 1.37 (95% CI 1.05-1.78), respectively. In trials comparing higher versus lower PEEP strategies, Powerelastic was increased in the higher PEEP arm (24 ± 1.7 vs 20 ± 1.5 J/min, respectively), whereas the other parameters were not affected on average by a higher PEEP ventilation strategy. CONCLUSIONS: In trials of lung-protective ventilation strategies, VT, ΔP, Powerelastic, Powerdynamic, and Powerdriving exhibited similar moderation of treatment effect on mortality. In this study, modified mechanical power did not add important information on the risk of death from VILI in comparison to VT or ΔP.

Acute Effects of Lung Expansion Maneuvers in Comatose Subjects With Prolonged Bed Rest.

BACKGROUND: Patients with decreased consciousness are prone to prolonged bed rest and respiratory complications. If effective in reducing atelectasis, lung expansion maneuvers could be used to prevent these complications. In comatose, bedridden subjects, we aimed to assess the acute effect on regional lung aeration of 2 lung expansion techniques: expiratory positive airway pressure and the breath-stacking maneuver. Our secondary aim was to evaluate the influence of these lung expansion techniques on regional ventilation distribution, regional ventilation kinetics, respiratory pattern, and cardiovascular system. METHODS: We enrolled 10 subjects status post neurosurgery, unable to follow commands, and with prolonged bed rest. All subjects were submitted to both expansion techniques in a randomized order. Regional lung aeration, ventilation distribution, and regional ventilation kinetics were measured with electrical impedance tomography. RESULTS: Lung aeration increased significantly during the application of both expiratory positive airway pressure and breath-stacking (P < .001) but returned to baseline values seconds afterwards. The posterior lung regions had the largest volume increase (P < .001 for groups). Both maneuvers induced asynchronous inflation and deflation between anterior and posterior lung regions. There were no significant differences in cardiovascular variables. CONCLUSIONS: In comatose subjects with prolonged bed rest, expiratory positive airway pressure and breath-stacking promoted brief increases in lung aeration. (ClinicalTrials.gov registration NCT02613832.).

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.