Physiological comparison of noninvasive ventilation and high-flow nasal oxygen on inspiratory efforts and tidal volumes after extubation: a randomized crossover trial

Critical Care volume 29, Article number: 185 Published: 08 May 2025

Background

Extubation failure leading to reintubation is associated with high mortality. In patients at high-risk of extubation failure, clinical practice guidelines recommend prophylactic non-invasive ventilation (NIV) over high-flow nasal oxygen (HFNO) immediately after extubation. However, the physiological effects supporting the beneficial effect of NIV have been poorly explored. We hypothesized that NIV may reduce patient inspiratory efforts to a greater extent than HFNO after extubation.

Methods

In a prospective physiological study, patients at high-risk of extubation failure (> 65 years old or underlying cardiac or respiratory disease) were included to receive after planned extubation prophylactic NIV and HFNO in a randomized crossover order, followed by standard oxygen. Inspiratory efforts were assessed by calculation of the simplified esophageal pressure–time-product per minute (sPTP_es in cmH₂O s/min). Tidal volumes, distribution and homogeneity of ventilation were estimated using electrical impedance tomography.

Results

Twenty patients were retained in the analysis. Inspiratory efforts were lower with NIV than with HFNO (sPTP_es 196 cm H₂O s/min [116–234] vs. 220 [178–327], p < 0.001) whereas tidal volumes were larger with NIV than with HFNO (8.4 mL/kg of predicted body weight [6.7–9.9] vs. 6.9 [5.3–8.6], p = 0.005). There was a non-significant increase in dorsal region ventilation under NIV compared to HFNO.

Conclusions

In patients at high-risk of extubation failure, prophylactic NIV significantly decreased inspiratory efforts with increased tidal volumes compared to HFNO. The clinical benefits of NIV to prevent reintubation in patients at high-risk may be mediated by these physiological effects.

 

Respiratory drive heterogeneity associated with systemic inflammation and vascular permeability in acute respiratory distress syndrome

 by Elias Baedorf-Kassis, Michael Murn, Amy L. Dzierba, Alexis L. Serra, Ivan Garcia, Emily Minus, Clarissa Padilla, Todd Sarge, Valerie M. Goodspeed, Michael A. Matthay, Michelle N. Gong, Deborah Cook, Stephen H. Loring, Daniel Talmor and Jeremy R. Beitler 

 Critical Care volume 28, Article number: 136, Published: 23 April 2024

Background

In acute respiratory distress syndrome (ARDS), respiratory drive often differs among patients with similar clinical characteristics. Readily observable factors like acid–base state, oxygenation, mechanics, and sedation depth do not fully explain drive heterogeneity. This study evaluated the relationship of systemic inflammation and vascular permeability markers with respiratory drive and clinical outcomes in ARDS.

Methods

ARDS patients enrolled in the multicenter EPVent-2 trial with requisite data and plasma biomarkers were included. Neuromuscular blockade recipients were excluded. Respiratory drive was measured as PES0.1, the change in esophageal pressure during the first 0.1 s of inspiratory effort. Plasma angiopoietin-2, interleukin-6, and interleukin-8 were measured concomitantly, and 60-day clinical outcomes evaluated.

Results

54.8% of 124 included patients had detectable respiratory drive (PES0.1 range of 0–5.1 cm H2O). Angiopoietin-2 and interleukin-8, but not interleukin-6, were associated with respiratory drive independently of acid–base, oxygenation, respiratory mechanics, and sedation depth. Sedation depth was not significantly associated with PES0.1 in an unadjusted model, or after adjusting for mechanics and chemoreceptor input. However, upon adding angiopoietin-2, interleukin-6, or interleukin-8 to models, lighter sedation was significantly associated with higher PES0.1. Risk of death was less with moderate drive (PES0.1 of 0.5–2.9 cm H2O) compared to either lower drive (hazard ratio 1.58, 95% CI 0.82–3.05) or higher drive (2.63, 95% CI 1.21–5.70) (p = 0.049).

Conclusions

Among patients with ARDS, systemic inflammatory and vascular permeability markers were independently associated with higher respiratory drive. The heterogeneous response of respiratory drive to varying sedation depth may be explained in part by differences in inflammation and vascular permeability.

 

Lung- and Diaphragm-Protective Ventilation by Titrating Inspiratory Support to Diaphragm Effort: A Randomized Clinical Trial

 

by de Vries, Heder J.; Jonkman, Annemijn H.; de Grooth, Harm J.; Duitman, Jan Willem.; Girbes, Armand R. J.; Ottenheijm, Coen A. C.; Schultz, Marcus J.; van de Ven, Peter M.; Zhang, Yingrui; de Man, Angelique M. E.; Tuinman, Pieter R.; Heunks, Leo M. A. 

 

Critical Care Medicine: February 2022 - Volume 50 - Issue 2 - p 192-203

 

OBJECTIVES: Lung- and diaphragm-protective ventilation is a novel concept that aims to limit the detrimental effects of mechanical ventilation on the diaphragm while remaining within limits of lung-protective ventilation. The premise is that low breathing effort under mechanical ventilation causes diaphragm atrophy, whereas excessive breathing effort induces diaphragm and lung injury. In a proof-of-concept study, we aimed to assess whether titration of inspiratory support based on diaphragm effort increases the time that patients have effort in a predefined “diaphragm-protective” range, without compromising lung-protective ventilation.

DESIGN: Randomized clinical trial.

SETTING: Mixed medical-surgical ICU in a tertiary academic hospital in the Netherlands.

PATIENTS: Patients (n = 40) with respiratory failure ventilated in a partially-supported mode. INTERVENTIONS: In the intervention group, inspiratory support was titrated hourly to obtain transdiaphragmatic pressure swings in the predefined “diaphragm-protective” range (3–12 cm H2O). The control group received standard-of-care.

MEASUREMENTS AND MAIN RESULTS: Transdiaphragmatic pressure, transpulmonary pressure, and tidal volume were monitored continuously for 24 hours in both groups. In the intervention group, more breaths were within “diaphragm-protective” range compared with the control group (median 81%; interquartile range [64–86%] vs 35% [16–60%], respectively; p < 0.001). Dynamic transpulmonary pressures (20.5 ± 7.1 vs 18.5 ± 7.0 cm H2O; p = 0.321) and tidal volumes (7.56 ± 1.47 vs 7.54 ± 1.22 mL/kg; p = 0.961) were not different in the intervention and control group, respectively.

CONCLUSIONS: Titration of inspiratory support based on patient breathing effort greatly increased the time that patients had diaphragm effort in the predefined “diaphragm-protective” range without compromising tidal volumes and transpulmonary pressures. This study provides a strong rationale for further studies powered on patient-centered outcomes.