Intracranial response to positive end-expiratory pressure is influenced by lung recruitability and gas distribution during mechanical ventilation in acute brain injury patients: a proof-of-concept physiological studyShow others and affiliations
2025 (English)In: Intensive Care Medicine Experimental, E-ISSN 2197-425X, Vol. 13, no 1, article id 43Article in journal (Refereed) Published
Abstract [en]
Background
The effect of positive end-expiratory pressure (PEEP) on intracranial pressure (ICP) dynamics in patients with acute brain injury (ABI) remains controversial. PEEP can benefit oxygenation by promoting alveolar recruitment, but its influence on ICP is complex. The primary aims of this study were to investigate 1) how lung recruitability influences oxygenation and 2) how lung recruitability and regional gas distribution, measured via recruitment-to-inflation (RI) ratio and electrical impedance tomography (EIT), affect ICP in response to PEEP changes in critically ill patients in their early phase of ABI.
Methods
Ten mechanically ventilated ABI patients were included. Pressure reactivity index (PRx) was estimated. Using RI manoeuvre and EIT, lung recruitability and gas distribution were assessed in response to a standardised PEEP change (from high to low levels, with a delta of 10 cmH2O). Changes in ICP (ΔICP) were calculated between high and low PEEP. Lung inhomogeneity indices (global inhomogeneity index [GI] and local inhomogeneity index [LI]) were derived from EIT. Correlations between ventilatory variables and ICP were analysed.
Results
Blood oxygenation significantly decreased, going from high (14 [IQR: 12–15] cmH₂O) to low (4 [IQR: 2–5] cmH₂O) PEEP. Reducing PEEP significantly increased ICP (from 9 [IQR: 5–13] to 12 [IQR: 8–16] mmHg, p < 0.01), while cerebral perfusion pressure (CPP) improved (from 71 [IQR:67–83] to 75 [IQR: 70–84] mmHg, p = 0.03) and mean arterial pressure (MAP) increased (from 79 [IQR: 69–95] to 84 [IQR: 76–99] mmHg, p < 0.01). The RI ratio correlated significantly with ΔICP (rho = 0.87, p < 0.01), as did Vrec% (proportion of recruited volume, rho = 0.65) and GI (rho = 0.5). LI did not correlate with ΔICP. PRx was 0.30 [IQR: 0.12–0.42], indicating a deranged cerebral autoregulation.
Conclusions
Patients with a higher potential for lung recruitability had a more beneficial effect of PEEP on oxygenation. These effects should be interpreted cautiously, given that lung recruitability and global inhomogeneity of gas distribution significantly influenced the intracranial response to PEEP in ABI patients. As indicated by MAP and CPP, PEEP may impact systemic haemodynamics and cerebral perfusion when cerebral autoregulation is deranged. These findings underscore the importance of multimodal (i.e. respiratory, cerebral and haemodynamics) monitoring for optimising ventilation strategies in ABI patients and provide a framework for future research.
Trial registration Registration number: NCT05363085, Date of registration: May 2022
Place, publisher, year, edition, pages
Springer, 2025. Vol. 13, no 1, article id 43
Keywords [en]
Acute brain injury, Mechanical ventilation, Lung-brain interaction, Intracranial pressure, Lung mechanics
National Category
Anesthesiology and Intensive Care Neurology
Identifiers
URN: urn:nbn:se:uu:diva-555359DOI: 10.1186/s40635-025-00750-yISI: 001466690700001PubMedID: 40229445Scopus ID: 2-s2.0-105002909863OAI: oai:DiVA.org:uu-555359DiVA, id: diva2:1955221
Part of project
Microscopic dynamic tidal changes in lung acini in lung disease models, studied in vivo by synchrotron radiation computed tomography, positron emission tomography and magnetic resonance imaging, Swedish Research CouncilVentilator induced lung injury: translational and clinical studies, Swedish Heart Lung FoundationVentilator induced lung injury: translational and clinical studies, Swedish Heart Lung Foundation
Funder
Swedish Heart Lung Foundation, 20220536Swedish Heart Lung Foundation, 20200877Swedish Heart Lung Foundation, 20200825Swedish Heart Lung Foundation, 20220681Swedish Heart Lung Foundation, 20230767Swedish Research Council, 2018-02438Swedish Society for Medical Research (SSMF), 463402221Swedish Society for Medical Research (SSMF), SG-22–0086-H-03Swedish Society of Medicine, SLS-959793Stiftelsen A Gullstrands fond, ALF-977974Stiftelsen A Gullstrands fond, ALF-977586Stiftelsen A Gullstrands fond, ALF-938050
Note
De två första författarna delar förstaförfattarskapet
2025-04-292025-04-292025-04-29Bibliographically approved