Evidence map›Paper›PMID 28403909›Full record

ReviewCritical care (London, England)2017

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a "two-hit" model.

Mypinder S Sekhon, Philip N Ainslie, Donald E Griesdale

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Critical care (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04563000 (Impact of Vitamin C on Biomarkers of Neurologic Injury in Patients With Return of Spontaneous Circulation After Out-of-Hospital Cardiac Arrest), which is not on this map. Cited by 298 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
298citing papers in PubMed, 10 pooled it
36.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT04563000 phase2unknown statusnot on this mapstarted 2020, after this paper: background citation

Impact of Vitamin C on Biomarkers of Neurologic Injury in Patients With Return of Spontaneous Circulation After Out-of-Hospital Cardiac Arrest

TypeinterventionalSponsorUniversity Medical Centre MariborRan2020 to 2022Enrolled150ConditionsHeart Arrest, Out-Of-Hospital, Biomarkers, Oxidative Stress, Neurological InjuryArmsVitamin C, Placebo
3 · Its place in the literature

Who cites it

298 citing papers in PubMed, 10 syntheses or guidelines pooled it, 573 citations in OpenAlex.

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  18. A cardiovascular-motor axis framework for perfusion-mediated motor impairment.International journal of cardiology. Heart & vasculature · 2026
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238 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Mypinder S SekhonDivision of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, University of British Columbia, Room 2438, Jim Pattison Pavilion, 2nd Floor, 855 West 12th Avenue, Vancouver, BC, V5Z 1M9, Canada. mypindersekhon@gmail.com.
Philip N AinslieCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan, Kelowna, BC, Canada.
Donald E GriesdaleDivision of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, University of British Columbia, Room 2438, Jim Pattison Pavilion, 2nd Floor, 855 West 12th Avenue, Vancouver, BC, V5Z 1M9, Canada.
University of British Columbia · CAVancouver Coastal Health · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia.Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications.We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA. Potential therapeutic targets and future research directions are summarized.

Indexed as

BrainCerebrovascular CirculationHeart ArrestHumansHyperthermia, InducedHypoxia, BrainReperfusion InjuryAnemiaCarbon dioxideCardiac arrestCerebral edemaCerebral oxygen deliveryHypothermiaHypoxic ischemic brain injuryNormobaric hyperoxiaTargeted temperature management

Identifiers

PMID28403909
PMCPMC5390465
OpenAlexW2607155970

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.