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.
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