ArticleJournal of clinical monitoring and computing2026
Cerebral monitoring responses to bedside physiological challenges in comatose post-cardiac arrest patients.
Article in Journal of clinical monitoring and computing, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To evaluate the effects of three simple bedside challenges on cerebral oxygenation and brain activity, measured non-invasively using near-infrared spectroscopy (NIRS) and frontal single-channel electroencephalography (EEG), in comatose post-cardiac arrest patients, and to examine whether these responses differ according to cerebral autoregulation status and intensive care unit (ICU) outcome and could aid early prognostication. Three bedside physiological challenges were conducted: (1) increasing the fraction of inspired oxygen (FiO₂) to 100%, (2) lowering the head-of-bed (HOB) to 0°, and (3) elevating end-tidal carbon dioxide (etCO₂) by 1.0 kPa. Tissue oxygen saturation (StO₂) and EEG amplitude were hypothesized to increase, by enhancing oxygen delivery (FiO₂), augmenting cerebral perfusion pressure (HOB), and inducing cerebral vasodilation (etCO₂). Furthermore, we examined the associations between signal responses, cerebral autoregulation status, and ICU outcome. Of the 48 monitored patients, FiO
Indexed as
Identifiers
41369879What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.