ReviewJournal of clinical monitoring and computing2015
Monitoring CO2 in shock states.
Review in Journal of clinical monitoring and computing, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed, 14 citations in OpenAlex.
- Use of COAnnals of intensive care · 2025Review
- Optimal Perfusion Targets in Cardiogenic Shock.JACC. Advances · 2022Review
- The venous-arterial difference in COJournal of clinical monitoring and computing · 2017Article
- High veno-arterial carbon dioxide gradient is not predictive of worst outcome after an elective cardiac surgery: a retrospective cohort study.Journal of clinical monitoring and computing · 2016Observational
- Journal of Clinical Monitoring and Computing 2015 end of year summary: cardiovascular and hemodynamic monitoring.Journal of clinical monitoring and computing · 2016Review
- Journal of Clinical Monitoring and Computing 2015 end of year summary: respiration.Journal of clinical monitoring and computing · 2016Review
- The utility of monitoring end-tidal carbon dioxide in emergency department to predict inhospital mortality of patients presenting with nontraumatic shock: A prospective observational study.Turkish journal of emergency medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The primary end point when treating acute shock is to restore blood circulation, mainly by reaching macrocirculatory parameters. However, even if global haemodynamic goals can be achieved, microcirculatory perfusion may remain impaired, leading to cellular hypoxia and organ damage. Interestingly, few methods are currently available to measure the adequacy of organ blood flow and tissue oxygenation. The rise in tissue partial pressure of carbon dioxide (CO2) has been observed when tissue perfusion is decreased. In this regard, tissue partial pressure of CO2 has been proposed as an early and reliable marker of tissue hypoxia even if the mechanisms of tissue partial pressure in CO2 rise during hypoperfusion remain unclear. Several technologies allow the estimation of CO2 content from different body sites: vascular, tissular (in hollow organs, mucosal or cutaneous), and airway. These tools remain poorly evaluated, and some are used but are not widely used in clinical practice. The present review clarifies the physiology of increasing tissue CO2 during hypoperfusion and underlines the specificities of the different technologies that allow bedside estimation of tissue CO2 content.
Indexed as
Identifiers
What 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.